扁平苔藓临床病理分析与免疫病理发病机制初步研究
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摘要
目的:
(1)研究扁平苔藓临床病理特征,为进一步探讨扁平苔藓的发病机制及指导其治疗提供依据;
(2)探讨炎性细胞因子(TNF-α、ICAM-1)、凋亡相关蛋白(Caspase-3、Bax)、细胞周期蛋白(Cyclin D1)及Th1型细胞因子(IL-12)在扁平苔藓患者中的表达及临床意义。
方法:
(1)回顾2005年1月至2007年12月在华中科技大学同济医学院附属协和医院皮肤科经临床、病理确诊为扁平苔藓患者83例,结合所选研究对象的临床资料和病理资料,按不同条件分组,进行临床和病理资料分析;
(2)采用免疫组化SP法对29例扁平苔藓患者皮损组织和10正常人皮肤组织中TNF-α、ICAM-1、Caspase-3、Bax、Cyclin D1蛋白表达水平进行检测;
(3)采用逆转录聚合酶链反应(RT-PCR)方法对29例扁平苔藓患者皮损组织和10例正常人皮肤组织中IL-12p40mRNA、IL-12p35mRNA的表达水平进行检测;
(4)分离29例扁平苔藓患者和10例正常人外周血单个核细胞(PBMC),检测PBMC培养上清液中IL-12蛋白水平。
结果:
(1)83例扁平苔藓患者临床病理分析结果
①一般资料:发病男女无性别差异(χ2=0.11,P>0.05),男女比例为1.08:1,平均年龄为42.84±15.97岁;以30-39岁年龄之间最多;平均病程33.54月;病程<1年组与≥1年组比较,差异无统计学意义(χ2=0.51,P>0.05);
②发病部位以两处或两处以上同时受累最多见,占34.94%;其次为口腔和四肢受累,各占19.28%;躯干和臀、腹股沟、外生殖器受累各占12.05%;面部受累最少,占2.40%。组间比较,差异有统计学意义(χ2=29.55,P<0.05);
③皮损以紫红色、紫褐色丘疹、斑片者最多,占61.45%;以糜烂、溃疡为主者占12.05%;灰黑色、灰青色、灰褐色丘疹、斑片为主者占7.23%;其它少见非典型皮疹占19.27%。组间比较,差异有统计学意义(χ2=61.24,P <0.05);
④67.47%的患者无自觉症状或症状轻微,不影响正常工作和学习,27.71%的患者诉严重瘙痒,4.82%患者疼痛症状明显。组间比较,差异有统计学意义(χ2=50.05,P<0.05);
⑤100%病例病理象示基底细胞液化变性和真皮浅层炎症细胞浸润;54.22%病例见胶样小体形成;63.86%的病例存在明显表皮病理学改变;3.61%出现表皮下裂隙或水疱;
⑥首诊即靠临床特点即可确诊扁平苔藓44例,仅占53.10%。
(2)TNF-α蛋白在扁平苔藓皮损组织和正常人皮肤组织中的表达
29例扁平苔藓皮损组织中,TNF-α阳性表达率为93.10%,10例正常人皮肤组织中TNF-α阳性表达率仅为30.00%,组间比较差异有统计学意义(χ2=19.40,P<0.05)。
(3)ICAM-1在扁平苔藓皮损组织和正常人皮肤组织中的表达
29例扁平苔藓皮损组织中,ICAM-1阳性表达率为89.66%,10例正常人皮肤组织均未检测到ICAM-1阳性表达,阳性率为0.00%,组间比较,差异有统计学意义(χ~2=26.90,P<0.05)。
(4)Caspase-3在扁平苔藓皮损组织和正常人皮肤组织中的表达
29例扁平苔藓皮损组织中,Caspase-3阳性表达率为86.20%,10例正常皮肤组织中,Caspase-3阳性表达率为20.00%,组间比较,差异有统计学意义(χ2=14.15,P<0.05)。
(5)Bax在扁平苔藓皮损组织和正常人皮肤组织中的表达
29例扁平苔藓皮损组织中,Bax阳性表达率为93.10%,10例正常人皮肤组织中,Bax阳性表达率为50.00%,组间比较,差异有统计学意义(χ2=17.60,P<0.05)。
(6)Cyclin D1在在扁平苔藓皮损组织和正常人皮肤组织中的表达
29例扁平苔藓皮损组织中,Cyclin D1阳性表达率为79.31%,10例正常人皮肤组织中,Cyclin D1表达阳性率为30.00%,组间比较,差异有统计学意义(χ2=8.57,P<0.05)。
(7)IL-12p40mRNA在扁平苔藓皮损组织和正常人皮肤组织中的表达
29例扁平苔藓患者皮损处均表达IL-12p40mRNA,而10例正常皮肤组织均不能检测到IL-12p40mRNA,组间比较差异均有统计学意义(F=9.03,P<0.05)。
(8)IL-12p35mRNA在扁平苔藓皮损组织和正常人皮肤中的表达
29例扁平苔藓患者皮损组织和10例正常人皮肤组织中均表达IL-12p35 mRNA,但皮损组和正常对照组组间比较,无显著性差异(F=3.71,P>0.05)。
(9)IL-12蛋白在扁平苔藓患者和正常人外周血PBMC培养上清中的检测
29例扁平苔藓患者外周血PBMC培养上清液IL-12平均水平为57.14±19.64pg/mL,而10例正常对照组外周血PBMC培养上清IL-12平均水平为30.10±7.45pg/mL。两者比较,差异有统计学意义(F=5.75,P<0.05)。
结论:
(1)83例扁平苔藓患者以30-39岁年龄组发病最多;
(2)发病部位以两处或两处以上同时受累居多;临床表现多样,以紫红色、紫褐色丘疹、斑片者最多;患者多无自觉症状或症状轻微,不影响正常工作和学习;
(3)扁平苔藓病理特征为基底细胞液化变性和真皮浅层炎症细胞浸润;部分病例可见胶样小体形成、表皮病理学改变等;
(4)必须临床与病理相结合才能正确诊断扁平苔藓;
(5)TNF-α、ICAM-1在扁平苔藓皮损局部异常高表达,可能促进皮损局部慢性炎症发应,与扁平苔藓发病有关;
(6)Caspase-3、Bax在扁平苔藓皮损局部异常高表达,可能促进皮损局部角质形成细胞凋亡,与扁平苔藓发病有关;
(7)Cyclin D1在扁平苔藓皮损局部异常高表达,可能促进角质形成细胞细胞周期的进程,促进其增殖,可能有助于维持表皮形态的完整性,在机体抗扁平苔藓过程中发挥保护性作用;
(8)IL-12p40mRNA在扁平苔藓皮损局部异常高表达和外周血PBMC分泌IL-12增高,可能与扁平苔藓发病过程中Th1型自身免疫反应有关。
Objective:
(1)To study the clinical feature and pathologic character of lichen planus.
(2) To investigate the role of proinflammation cytokine (TNF-αand ICAM-1), apoptosis related protein (Caspase-3 and Bax), Cyclin D1, and Th1-type cytokine (IL-12) in the pathogenesis of lichen planus.
Methods:
(1) 83 lichen planus patients from Union hospital of Huazhong University of Science Technology which had been diagnosed by clinical character and skin biopsy between Jan 2005 and Dec 2007 were reviewed;
(2) Immunohistochemical technique was employed to observe the expression of TNF-α, ICMA-1, Caspase-3, Bax and Cyclin D1 in the lesional skin from 29 patients with lichen planus. Normal skin from 10 healthy persons was used as control;
(3) The expressions of IL-12p35 and IL-12p40 mRNA were semi-quantitatively analyzed with reverse transcriptase-polymerase chain reaction (RT-PCR) in the lesional skin from 29 patients with lichen planus and 10 healthy persons.
(4) PBMC was obtained from 29 patients with LP and 10 normal controls. IL-12 in the culture supernatants were measured quantitatively by ELISA.
Results:
(1) According to our information, the onset of LP generally occurred in the middle-aged especially 30-39 years old (mean age 42.84±15.97), with the ratio of male to female 1.08:1;
(2) The lesions always involved more than one part of body. The clinical character is diversifying, and prunosus papular and patch were the most clinical manifestations. Many patients were asymptomatic or symptomatic in low degree;
(3) The histopathology of LP is the subepithelial band-like inflammatory cell infiltrate predominated by lymphocytes, and destruction of the epithelial basal cell layer. In some cases, there is Civatte bodies and change in epidermal skin;
(4) Only depend on clinical character, the dermatologist can not diagnosis lichen planus correctly;
(5) Positive TNF-αexpressions rate in lichen planus were significantly higher than those in normal skins (χ~2=19.40,P<0.05);
(6) Positive ICAM-1 expressions rate in lichen planus were significantly higher than those in normal skins (χ~2=26.90,P<0.05);
(7) Positive Caspase-3 expressions rate in lichen planus were significantly higher than those in normal skins (χ~2=14.15,P<0.05);
(8) Positive Bax expressions rate in lichen planus were significantly higher than those in normal skins (χ~2=17.60,P<0.05);
(9) Positive Cyclin D1 expressions rate in lichen planus were significantly higher than those in normal skins (χ~2=8.57,P<0.05);
(10) The lever of IL-12p40mRNA in lichen planus were significantly higher than those in normal skins (F=9.03,P<0.05);
(11) There is no difference in the lever of IL-12p35mRNA of lichen planus and normal skins (F=3.71,P>0.05);
(12) IL-12 in the culture supernatants of PBMC from patients with lichen planus were significantly higher than those from normal controls (F=5.75,P<0.05).
Conclusions:
(1) According to our information, the onset of LP generally occurred in the middle-aged especially 30-39 years old (mean age 42.84±15.97), with the ratio of male to female 1.08:1;
(2) The lesions always involved more than one part of body. The clinical character is diversifying, and prunosus papular and patch were the most clinical manifestations. Many patients were asymptomatic or symptomatic in low degree;
(3) The histopathology of LP is the subepithelial band-like inflammatory cell infiltrate predominated by lymphocytes, and destruction of the epithelial basal cell layer. In some cases, there is Civatte bodies and change in epidermal skin;
(4) In order to diagnosis lichen planus correctly, the dermatologist must master the clinical and pathologic character of LP;
(5) The expression of TNF-αand ICAM-1 might play an important role in the chronic inflammation of lichen planus;
(6) The expression of Caspase-3 and Bax might play an important role in the keratinocyte apoptosis of lichen planus;
(7) The expression of Cyclin D1 might play an important role in the proliferation of keratinocyte in lichen planus;
(8) The overexpression of IL-12p40mRNA in lesional skin and IL-12 in the culture supernatants of PBMC might play an important role in the Th1-type autoimmunologic reaction of LP.
(1)研究扁平苔藓临床病理特征,为进一步探讨扁平苔藓的发病机制及指导其治疗提供依据;
(2)探讨炎性细胞因子(TNF-α、ICAM-1)、凋亡相关蛋白(Caspase-3、Bax)、细胞周期蛋白(Cyclin D1)及Th1型细胞因子(IL-12)在扁平苔藓患者中的表达及临床意义。
方法:
(1)回顾2005年1月至2007年12月在华中科技大学同济医学院附属协和医院皮肤科经临床、病理确诊为扁平苔藓患者83例,结合所选研究对象的临床资料和病理资料,按不同条件分组,进行临床和病理资料分析;
(2)采用免疫组化SP法对29例扁平苔藓患者皮损组织和10正常人皮肤组织中TNF-α、ICAM-1、Caspase-3、Bax、Cyclin D1蛋白表达水平进行检测;
(3)采用逆转录聚合酶链反应(RT-PCR)方法对29例扁平苔藓患者皮损组织和10例正常人皮肤组织中IL-12p40mRNA、IL-12p35mRNA的表达水平进行检测;
(4)分离29例扁平苔藓患者和10例正常人外周血单个核细胞(PBMC),检测PBMC培养上清液中IL-12蛋白水平。
结果:
(1)83例扁平苔藓患者临床病理分析结果
①一般资料:发病男女无性别差异(χ2=0.11,P>0.05),男女比例为1.08:1,平均年龄为42.84±15.97岁;以30-39岁年龄之间最多;平均病程33.54月;病程<1年组与≥1年组比较,差异无统计学意义(χ2=0.51,P>0.05);
②发病部位以两处或两处以上同时受累最多见,占34.94%;其次为口腔和四肢受累,各占19.28%;躯干和臀、腹股沟、外生殖器受累各占12.05%;面部受累最少,占2.40%。组间比较,差异有统计学意义(χ2=29.55,P<0.05);
③皮损以紫红色、紫褐色丘疹、斑片者最多,占61.45%;以糜烂、溃疡为主者占12.05%;灰黑色、灰青色、灰褐色丘疹、斑片为主者占7.23%;其它少见非典型皮疹占19.27%。组间比较,差异有统计学意义(χ2=61.24,P <0.05);
④67.47%的患者无自觉症状或症状轻微,不影响正常工作和学习,27.71%的患者诉严重瘙痒,4.82%患者疼痛症状明显。组间比较,差异有统计学意义(χ2=50.05,P<0.05);
⑤100%病例病理象示基底细胞液化变性和真皮浅层炎症细胞浸润;54.22%病例见胶样小体形成;63.86%的病例存在明显表皮病理学改变;3.61%出现表皮下裂隙或水疱;
⑥首诊即靠临床特点即可确诊扁平苔藓44例,仅占53.10%。
(2)TNF-α蛋白在扁平苔藓皮损组织和正常人皮肤组织中的表达
29例扁平苔藓皮损组织中,TNF-α阳性表达率为93.10%,10例正常人皮肤组织中TNF-α阳性表达率仅为30.00%,组间比较差异有统计学意义(χ2=19.40,P<0.05)。
(3)ICAM-1在扁平苔藓皮损组织和正常人皮肤组织中的表达
29例扁平苔藓皮损组织中,ICAM-1阳性表达率为89.66%,10例正常人皮肤组织均未检测到ICAM-1阳性表达,阳性率为0.00%,组间比较,差异有统计学意义(χ~2=26.90,P<0.05)。
(4)Caspase-3在扁平苔藓皮损组织和正常人皮肤组织中的表达
29例扁平苔藓皮损组织中,Caspase-3阳性表达率为86.20%,10例正常皮肤组织中,Caspase-3阳性表达率为20.00%,组间比较,差异有统计学意义(χ2=14.15,P<0.05)。
(5)Bax在扁平苔藓皮损组织和正常人皮肤组织中的表达
29例扁平苔藓皮损组织中,Bax阳性表达率为93.10%,10例正常人皮肤组织中,Bax阳性表达率为50.00%,组间比较,差异有统计学意义(χ2=17.60,P<0.05)。
(6)Cyclin D1在在扁平苔藓皮损组织和正常人皮肤组织中的表达
29例扁平苔藓皮损组织中,Cyclin D1阳性表达率为79.31%,10例正常人皮肤组织中,Cyclin D1表达阳性率为30.00%,组间比较,差异有统计学意义(χ2=8.57,P<0.05)。
(7)IL-12p40mRNA在扁平苔藓皮损组织和正常人皮肤组织中的表达
29例扁平苔藓患者皮损处均表达IL-12p40mRNA,而10例正常皮肤组织均不能检测到IL-12p40mRNA,组间比较差异均有统计学意义(F=9.03,P<0.05)。
(8)IL-12p35mRNA在扁平苔藓皮损组织和正常人皮肤中的表达
29例扁平苔藓患者皮损组织和10例正常人皮肤组织中均表达IL-12p35 mRNA,但皮损组和正常对照组组间比较,无显著性差异(F=3.71,P>0.05)。
(9)IL-12蛋白在扁平苔藓患者和正常人外周血PBMC培养上清中的检测
29例扁平苔藓患者外周血PBMC培养上清液IL-12平均水平为57.14±19.64pg/mL,而10例正常对照组外周血PBMC培养上清IL-12平均水平为30.10±7.45pg/mL。两者比较,差异有统计学意义(F=5.75,P<0.05)。
结论:
(1)83例扁平苔藓患者以30-39岁年龄组发病最多;
(2)发病部位以两处或两处以上同时受累居多;临床表现多样,以紫红色、紫褐色丘疹、斑片者最多;患者多无自觉症状或症状轻微,不影响正常工作和学习;
(3)扁平苔藓病理特征为基底细胞液化变性和真皮浅层炎症细胞浸润;部分病例可见胶样小体形成、表皮病理学改变等;
(4)必须临床与病理相结合才能正确诊断扁平苔藓;
(5)TNF-α、ICAM-1在扁平苔藓皮损局部异常高表达,可能促进皮损局部慢性炎症发应,与扁平苔藓发病有关;
(6)Caspase-3、Bax在扁平苔藓皮损局部异常高表达,可能促进皮损局部角质形成细胞凋亡,与扁平苔藓发病有关;
(7)Cyclin D1在扁平苔藓皮损局部异常高表达,可能促进角质形成细胞细胞周期的进程,促进其增殖,可能有助于维持表皮形态的完整性,在机体抗扁平苔藓过程中发挥保护性作用;
(8)IL-12p40mRNA在扁平苔藓皮损局部异常高表达和外周血PBMC分泌IL-12增高,可能与扁平苔藓发病过程中Th1型自身免疫反应有关。
Objective:
(1)To study the clinical feature and pathologic character of lichen planus.
(2) To investigate the role of proinflammation cytokine (TNF-αand ICAM-1), apoptosis related protein (Caspase-3 and Bax), Cyclin D1, and Th1-type cytokine (IL-12) in the pathogenesis of lichen planus.
Methods:
(1) 83 lichen planus patients from Union hospital of Huazhong University of Science Technology which had been diagnosed by clinical character and skin biopsy between Jan 2005 and Dec 2007 were reviewed;
(2) Immunohistochemical technique was employed to observe the expression of TNF-α, ICMA-1, Caspase-3, Bax and Cyclin D1 in the lesional skin from 29 patients with lichen planus. Normal skin from 10 healthy persons was used as control;
(3) The expressions of IL-12p35 and IL-12p40 mRNA were semi-quantitatively analyzed with reverse transcriptase-polymerase chain reaction (RT-PCR) in the lesional skin from 29 patients with lichen planus and 10 healthy persons.
(4) PBMC was obtained from 29 patients with LP and 10 normal controls. IL-12 in the culture supernatants were measured quantitatively by ELISA.
Results:
(1) According to our information, the onset of LP generally occurred in the middle-aged especially 30-39 years old (mean age 42.84±15.97), with the ratio of male to female 1.08:1;
(2) The lesions always involved more than one part of body. The clinical character is diversifying, and prunosus papular and patch were the most clinical manifestations. Many patients were asymptomatic or symptomatic in low degree;
(3) The histopathology of LP is the subepithelial band-like inflammatory cell infiltrate predominated by lymphocytes, and destruction of the epithelial basal cell layer. In some cases, there is Civatte bodies and change in epidermal skin;
(4) Only depend on clinical character, the dermatologist can not diagnosis lichen planus correctly;
(5) Positive TNF-αexpressions rate in lichen planus were significantly higher than those in normal skins (χ~2=19.40,P<0.05);
(6) Positive ICAM-1 expressions rate in lichen planus were significantly higher than those in normal skins (χ~2=26.90,P<0.05);
(7) Positive Caspase-3 expressions rate in lichen planus were significantly higher than those in normal skins (χ~2=14.15,P<0.05);
(8) Positive Bax expressions rate in lichen planus were significantly higher than those in normal skins (χ~2=17.60,P<0.05);
(9) Positive Cyclin D1 expressions rate in lichen planus were significantly higher than those in normal skins (χ~2=8.57,P<0.05);
(10) The lever of IL-12p40mRNA in lichen planus were significantly higher than those in normal skins (F=9.03,P<0.05);
(11) There is no difference in the lever of IL-12p35mRNA of lichen planus and normal skins (F=3.71,P>0.05);
(12) IL-12 in the culture supernatants of PBMC from patients with lichen planus were significantly higher than those from normal controls (F=5.75,P<0.05).
Conclusions:
(1) According to our information, the onset of LP generally occurred in the middle-aged especially 30-39 years old (mean age 42.84±15.97), with the ratio of male to female 1.08:1;
(2) The lesions always involved more than one part of body. The clinical character is diversifying, and prunosus papular and patch were the most clinical manifestations. Many patients were asymptomatic or symptomatic in low degree;
(3) The histopathology of LP is the subepithelial band-like inflammatory cell infiltrate predominated by lymphocytes, and destruction of the epithelial basal cell layer. In some cases, there is Civatte bodies and change in epidermal skin;
(4) In order to diagnosis lichen planus correctly, the dermatologist must master the clinical and pathologic character of LP;
(5) The expression of TNF-αand ICAM-1 might play an important role in the chronic inflammation of lichen planus;
(6) The expression of Caspase-3 and Bax might play an important role in the keratinocyte apoptosis of lichen planus;
(7) The expression of Cyclin D1 might play an important role in the proliferation of keratinocyte in lichen planus;
(8) The overexpression of IL-12p40mRNA in lesional skin and IL-12 in the culture supernatants of PBMC might play an important role in the Th1-type autoimmunologic reaction of LP.
引文
1 Thornhill MH. Immune mechanisms in oral lichen planus. Acta Odontol Scand, 2001, 59(3): 174-177.
2王椿森,李家文,等.皮肤性病免疫学.武汉:湖北科学技术出版社, 1999, 229-234.
3 Sugerman PB, Savage NW, Walsh LJ, et al. The pathogenesis of oral lichen planus. Crit Rev Oral Biol Med, 2002, 13(4): 350-365.
4 Walsh LJ, Savage NW, Ishii T, et al. Immunopathogenesis of oral lichen planus. J Oral pathol Med, 1990, 19(9): 389-396.
5赵辩.临床皮肤病学,第3版,南京:江苏科学技术出版社, 2001, 782-789
6 Bascones-Ilundain C, Gonzalez-Moles MA, Esparza-Gomez G, et al. Importance of apoptotic mechanisms in inflammatory infiltrate of oral lichen planus lesions. Anticancer Res, 2006, 26(1A): 357-362.
7 Weedon D, Searle J, Kerr JF. Apoptosis. Its nature and implications for dermatopathology. Am J dermatopathol, 1979, 1(2): 133-144.
8 Bloor BK, Malik FK, Odell EW, et al. Quantitative assessment of apoptosis in oral lichen planus, Oral Surg Oral Med Oral Pathol Radiol Endod, 1999, 88(2): 187-195.
9 Tobon-Arroyaye SI, Villegas-Acosta FA, Ruiz-Restrepo SM, et al. Expression of caspase-3 and structural changes associated with apoptotic cell death of keratincytes in oral lichen planus. Oral Dis, 2004, 10(3): 173-178.
10李鑫,丁政云,刘丽娟. 35例扁平苔藓临床和组织病理分析.中国麻风皮肤病杂志, 2007, 23(8): 686-687
11 Kyriakis KP, Terzoudi S, Palamaras I, et al. Sex and age distribution of patients with lichen planus. J Eur Acad Dermatol Venereol, 2006, 20(5): 302-626.
12吴志华.现代皮肤性病学,第1版,广州:广东人民出版社, 2000, 470-473.
1 Thornhill MH. Immune mechanisms in oral lichen planus. Acta Odontol Scand, 2001, 59(3): 174-177.
2 Dissemond J, Schroter S, Franckson T, et al. Pimecrolimus in an adhesive ointment as a new treatment option for oral lichen planus. Br J Dermatol, 2004, 150(4): 782-784.
3朱学骏、涂平.皮肤病的组织病理诊断.第2版.北京:北京医科大学出版社, 2001. 138.
4 Prpic Masssari L, Kastelan M, Cruber F, et al. Perforin expression in peripheral blood lymphocytes and skin-infiltrating cells in patients with lichen planus. Br J Dermatol, 2004; 151(2): 433-439
5 Sklavounou A, Chrysomali E, Scorilas A, et al. TNF-alpha expression and apoptosis-regulating proteins in oral lichen planus: a comparative immunohistochemical evaluation. J Oral Pathol Med, 2000, 29(8): 370-375.
6苏有明,于民,阎锋,等.限局性硬皮病血清sIL-2R、TNF-α水平和T淋巴细胞亚群的检测.临床皮肤科杂志, 1998, 27: 8-10.
7聂本勇,郑茂荣,范表源. TNF-α和IL-1β对HaCaT细胞诱生型一氧化氮合酶表达的影响.中国皮肤性病学杂志, 2004, 18: 68-70.
8陈建粮.细胞间粘附分子1表达的调控.国外医学免疫学分册, 2000, 23: 272-274.
9李红文,丁一,邓新国,等. ICAM-1、IGF-1在银屑病皮损中的表达.中国皮肤性病学杂志, 2001, 15: 297-298.
10狄正鸿,许静.扁平苔藓皮损中浸润淋巴细胞的研究.中国医科大学学报, 2006,35(4): 427-428.
11 Iijima W, Ohtani H, Nakayama T, et al. Infliltrating CD8+ T cells in oral lichen planus predominantly express CCR5 and CXCR3 and carry respective chemokine ligands RANTES/CCL5 and IP-10/CXCL10 in their cytolytic granules: a potential self -recruiting mechanism. Am J Pathol, 2003, 163(1): 261-268.
12 al-Janadi M, al-Balla S, al-Dalaan A, et al. Cytokine profile in systemic lupus erythematosus, rheumatoid arthritis, and other rheumatic diseases. J Clin Immunol, 1993, 13(1): 58-67.
13 Kono T, Tanii T, Furukawa M, et al. Effects of human recombinant tumor necrosis factor-alpha (TNF-alpha) on the proliferative potential of human keratinocytes cultured in serum-free medium. J Dermatol, 1990, 17(7): 409-413.
14 Farrell AM, Dean D, Millard PR, et al. Cytokine alterations in lichen sclerosus: an immunohistochemical study. Br J Dermatol, 2006, 155(5): 931-940.
15 Sugerman PB, Savage NW, Zhou X, et al. Oral lichen planus. Clin Dermatol, 2000, 18(5): 533-539.
16 Johansen C, Funding AT, Otkjaer K, et al. Protein expression of TNF-alpha in psoriatic skin is regulated at a posttranscriptional level by MAPK-activated protein kinase 2. J Immunol, 2006, 176(3): 1431-1438.
17 Sklavounou A, Chrysomali E, Scorilas A, et al. TNF-alpha expression and apoptosis-regulating proteins in oral lichen planus; a comparative immunohistochemical evaluation. J Oral Pathol Med, 2000, 29(8): 370-375.
18陈莉芬,李荣亨.肿瘤坏死因子α在肾脏疾病中的研究进展.国外医学泌尿系统分册, 2001, 21(4):147-149.
19 Beamer NB, Coull BM, Clark WM, et al. Interleukin-6 and interleukin-1 receptor antagonist in acute stroke. Ann Neurol, 1995, 37(6): 800-805.
20 Fassbender K, Rossol S, Kammer T, et al. Proinflammatory cytokines in serum of patients with acute cerebral ischemia: kinetics of sectetion and relation to the extent ofbrain damage and outcome of disease. J Neurol Sci, 1994, 122(2): 135-139.
21 Diamond MS, Staunton DE, Marlin SD, et al. Binding of the integrin Mac-1 (CD11b/CD18) to the third immunoglobulin-like domain of ICAM-1 (CD54) and its regulation by glycosylation. Cell, 1991, 65(6): 961-971.
22 Marlin SD, Stauton DE, Springer TA, et al. A soluble form of intercellular adhesion molecule-1 inhibits rhinovirus infection. Nature, 1990, 344(6261): 70-72.
23于新波,杨丕山.细胞间粘附分子-1在牙周炎中作用的研究现状.国外医学口腔医学分册, 2002, 29(6): 340-342.
24 Hagi-Pavli E, Farthing PM, Henshaw FN, et al. Presentation of ICAM-1 protein at the cell surface of oral keratinocytes in the presence of adrenomedullin and corticotrophin. Cell Physiol Biochem, 2005, 15(1-4): 167-174.
25 Carrozzo M, Uboldi de Capei M, Dametto E, et al. Tumor necrosis factor-alpha and interferon-gamma polymorphisms contribute to susceptibility to oral lichen planus. J Invest Dermatol, 2004, 122(1): 87-94.
1 Earnshaw WC, Martins LM, Kaufmann SH, et al. Mammalian caspase: structure, activation, substrates, and functions during apoptosis. Annu Rev Biochem, 1999, 68: 383-424.
2 Ferrer I, Planas AM. Signaling of cell death and cell survival following focal cerebral ischemia: life and death struggle in the penumbra. J Neuropathol Exp Neurol, 2003, 62(4): 329-339.
3 Zhang F, Yin W, Chen J. Apoptosis in cerebral ischemia: executional and regulatory signaling mechanisms. Neurol Res, 2004, 26(8): 835-845.
4 Plesnila N, Zhu C, Culmsee C, et al. Nuclear translocation of apoptosis-inducing factor after focal cerebral ischemia. J Cereb Blood Flow Metab, 2004, 24(4): 458-466.
5 Dekker NP, Lozada-Nur F, Lagenaur LA, et al. Apoptosis associated markers in orallichen planus. J Oral Pathol Med, 1997, 26(4): 170-175.
6 Neppelberg E, Johannessen AC, Jonsson R. Apoptosis in oral lichen planus. Eur J Oral Sci, 2001, 109(5): 361-364.
7 Li MH, Ito D, Sanada M, et al. Effect of 5-fluorouracil on G1 phase cell cycle regulation in oral cancer cell lines. Oral Oncol, 2004, 40(1): 63-70.
8 Villarroel Dorrego M, Correnti M, et al. Oral lichen planus: immunohistology of mucosal lesions. J Oral Pathol Med, 2002, 31(7): 410-414.
9 Bascones C, Gonzalez-Moles MA, Esparza G, et al. Apoptosis and cell cycle arrest in oral lichen planus Hypothesis on their possible influence on its malignant transformation. Arch Oral Biol, 2005, 50(10): 873-881.
10 Kerr JF, Wyllie AH, Currie AR. Apoptosis: a basic biological phenomenon with wide-rageing implication in tissue kenetics. Br J Cancer, 1972, 26(4): 239-257.
11 Suzuki A, Iwsaki M, Wagai N, et al. Involvement of cytoplasmic serine proteinase and CPP32 subfamily in the molecular machinery of Caspase-3 activiation during Fas-mediated apoptosis. Exp Cell Res, 1997, 233(1): 48-55.
12 Nicholson DW, Ali A, Thornberry NA, et al Identification and inhibition of the ICE/CED-3 protease necessary for mammalian apoptosis. Nature, 1995, 376(6535): 37-43.
13 Saikumar P, Dong Z, Mikhailov V, et al. Apoptosis: definition, mechanism, and relevance to disease. Am J Med, 1999, 107(5): 489-506.
14 Roy S, Bayly CI, Gareau Y, et al. Maintenance of caspase-3 proenzyme dormancy by an intrinsic“safety catch”regulatory tripeptide. Proc Natl Acad Sci USA, 2001, 98(11): 6132-6137.
15 Sklavounou A, Chrysomali E, Scorilas A, et al. TNF-alpha expression and apoptosis-regulating proteins in oral lichen planus: a comparative immunohistochemical evaluation. J Oral Pathol Med, 2000, 29(8): 370-375.
16 Khan A, Farah CS, Savage NW, et al. Th1 cytokines in oral lichen planus. J OralPathol Med, 2003, 32(2): 77-83.
17 Sugerman PB, Savage NW, Zhou X, et al. Oral lichen planus, Clin Dermatol, 2000, 18: 533-539.
18 Tobon-Arroyave SI, Villegas-Acosta FA, Ruiz-Restrepo SM, et al. Expression of caspase-3 and structural changes associated with apoptotic cell death of keratinocytes in oral lichen planus. Oral Dis, 2004, 10(3): 173-178.
19 Nicholson DW, Thornberry NA. Apoptosis. Life and death decisions. Science, 2003, 299(6504): 214-215.
20陈彦灵,童坦君.细胞凋亡是半胱天冬酶参与的复杂过程.生命科学, 2000, 20(2): 77-79.
21 Luo C, Zhu C, Jiang J, et al. Alterations of bcl-2, bcl-x and bax protein expressions in area CA-3 of rat hippocampus following fluid percussion brain injury. Chin J Traumatol, 1999, 2(2): 101-104.
22 Oltvai ZN, Mlilliman CL, Korsmeyer SJ. Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death. Cell, 1993, 74(4); 609-619.
23 Borner C. The Bcl-2 protein family: sensors and checkpoints for life-or-death decisions. Mol Immunol, 2003, 39(11): 615-647.
24孙红,惠延年,王立勤,等. Caspase-3和bax在视网膜母细胞瘤中的表达.第四军医大学学报2003; 24: 1162-1163
1 Dekker NP, Lozada-Nur F, Lagenaur LA, et al. Apoptosis-associated markers in oral lichen planus. J Oral Pathol Med, 1997, 26(4): 170-175.
2 Neppelberg E, Johannessen AC, Jonsson R. Apoptosis in oral lichen planus. Eur J Oral Sci, 2001, 109(5): 361-364
3 Walsh LJ, Savage NW, Ishii T, et al. Immunopathogenesis of oral lichen planus. J Oral Pathol Med, 1990, 19(9): 389-396.
4 Majorana A, Facchetti F, Pellegrini W, et al. Apoptosis-associated markers in oral lichen planus. J Oral Pathol Med, 1999, 28(1): 47-48.
5 Li MH, Ito D, Sanada M, et al. Effect of 5-fluorouracil on G1 phase cell cycle regulation in oral cancer cell lines. Oral Oncol, 2004, 40(1): 63-70.
6 Bloor BK, Malik FK, Odell EW, et al. Quantitative assessment of apoptosis in oral lichen planus, Oral Surg Oral Med Oral Pathol Radiol Endod, 1999, 88(2): 187-195.
7 Tobon-Arroyave SI, Villegas-Acosta FA, Ruiz-Restrepo SM, et al. Expression of caspase-3 and structural changes associated with apoptotic cell death of keratincytes in oral lichen planus. Oral Dis, 2004, 10(3): 173-178.
8 Motokura T, Bloom T, Kim HG, et al. A novel cyclin encoded by a bcl1-linked candidate oncogene. Nature, 1991, 350(6318): 512-515.
9 Xiong Y, Connolly T, Futcher B, et al. Human D-type cyclin. Cell, 1991, 65(4): 691-699.
10 Hunter T, Pines J. Cyclins and cancer II: Cyclin D and CDK inhibitors come of age. Cell, 1994, 79(4): 573-582.
11 Sherr CJ. G1 phase progression: Cycling on cue. Cell, 1994, 79(4): 551-555.
12 Gonzalez-Moles MA, Bascones-Ilundain C, Gil Montoya JA, et al. Cell cycle regulation mechanisms in oral lichen planus: molecular bases in epithelium predisposed to malignant transformation. Arch Oral Biol, 2006, 51(12): 1093-1103.
13 Tipoe GL, Jin V, White FH. The relationship between vascularity and cell proliferation in human normal and pathological lesions of the oral cheek epithelium. Eur J Cancer B Oral Oncol, 1996: 32B(1), 24-31.
14 Acay RR, Felizzola CR, de Araujo N, et al. Evaluation of proliferative potential in oral lichen planus and oral lichenoid lesions using immunohistochemical expression of p53 and Ki67. Oral Oncol, 2006, 42(5): 475-480.
15王业东,王林杰,王松山,等.慢性肝炎和原发性肝癌肝组织P21和P15蛋白的表达及与细胞凋亡的关系.中华实验和临床病毒学杂志, 2000, 14(2): 157-159.
16 Bascones C, Gonzalez-Moles MA, Esparza G, et al. Apoptosis and cell cycle arrest in oral lichen planus Hypothesis on their possible influence on its malignant transformation. Archives of Oral Biology, 2005, 50(10): 873-881.
1.陈敬,董德琼,杨渝浩.白介素-12与结核病.国外医学呼吸系统分册, 2002, 22(4): 220-222.
2. Simark-Mattsson C, Jontell M, Bergenholtz G, et al. Distribution of interferon-gamma mRNA-positive cells in oral lichen planus lesions. J Oral Pathol Med, 1998, 27(10): 483-488.
3. Simark-Mattsson C, Bergenholtz G, Jontell M, et al. Distribution of interleukin-2, -4, -10, tumour necrosis factor-alpha and transforming growth factor-beta mRNA in oral lichen planus. Arch Oral Biol, 1999, 44(6): 499-507.
4.郭海建,刘断民,刘俊,等.溃疡性结肠炎患者PBMC体外白细胞介素12诱生水平研究.实用临床医药杂志, 2007, 11(5): 65-67
5.吴雄文,梁智辉.实用免疫学实验技术,第1版,武汉:湖北科学技术出版社, 2002, 124-125.
6.唐皓,马中富.白介素-12的研究新进展.国外医学临床生物化学与检验学分册, 2001, 22(4): 177-178.
7. Trinchieri G. Interleukin-12 and the regulation of innate resistance and adaptive immunity. Nat Rev Immunol, 2003, 3(2): 133-146.
8. Schakel K, von Kietzell M, Hansel A, et al. Human 6-Sulfo LacNAc-expressing dendritic cells are principal producers of early interleukin-12 and are controlled by erythrocytes. Immunity, 2006, 24(6): 767-777.
9. Huang Q, Liu D, Majewski P, et al. The plasticity of dendritic cell responses to pathogens and their components. Science, 2001, 294(5543): 870-875.
10. Yu Y, Tang L, Wang J, et al. Psoriatic lesional keratinocytes promote the maturation of human monocyte-derived Langerhans cells. Dermatology, 2002, 204(2): 94-99.
11. Leung BP, McInnes IB, Esfandiari E, et al. Combined effects of IL-12 and IL-18 on the induction of collagen-induced arthritis. J Immunol, 2000, 164(12): 6495-6502.
12. Yano S, Komine M, Fujimoto M, et al. Interleukin 15 induces the signals of epidermal proliferation through ERK and PI3-kinase in a human epidermal keratinocyte cell line, HaCaT. Biochem Biophys Res Commun, 2003, 301(4): 841-847.
13.徐钰,高占成.白介素-12在支气管哮喘中的作用机制.国外医学呼吸系统分册, 2002, 22(6): 289-296.
14. Wenzel J, Scheler M, Proelss J et al. TypeⅠinterferon-associated cytotoxic inflammation in lichen planus. J Cutan Pathol, 2006, 33(1): 672-678.
15. Nestle FO, Conrad C. The IL-12 family member p40 chain as a master switch and novel therapeutic target in psoriasis. J Invest Dermatol, 2004, 123(6): xiv-xv.
16.狄正鸿,许静.扁平苔藓皮损中浸润淋巴细胞的研究.中国医科大学学报, 2006, 35(4): 427-428.
17. Simark-Mattsson C, Jontell M, Bergenholtz G, et al. Distribution of interferon-gamma mRNA-positive cells in oral lichen planus lesions. J Oral Pathol Med, 1998, 27(10): 483-488.
18. Simark-Mattsson C, Bergenholtz G, Jontell M, et al. Distribution of interleukin-2, -4, -10, tumour necrosis factor-alpha and transforming growth factor-beta mRNA in oral lichen planus. Arch Oral Biol, 1999, 44(6): 499-507.
1. Kyriakis KP, Terzoudi S, Palamaras I, et al. Sex and age distribution of patients with lichen planus. J Eur Acad Dermatol Venereol, 2006, 20(5): 302-626.
2. Calnan CD, Meara RH. St John’s Hospital diagnostic index. Trans Rep St John’s Hosp Derm Soc Lond, 1957, 39: 56-68
3. Depaoli M. Lichen rubber planus, clinical and statistical features. Minerva Dermatol, 1964, 39: 166-171.
4. Schmidt H. Frequency, duration and localization of lichen planus. A study based on 181 patients. Acta Derm Venereol, 1961, 41: 164-167.
5. Ikeda N, Ishii T, Iida S, et al. Epidemiological study of oral leukoplakia based on mass screening for oral mucosal diseases in a selected Japanese population. Community Dent Oral Epidemiol, 1991, 19(3): 160-163.
6. Murti PR, Daftary DK, Bhonsle RB, et al. Malignant potential of oral lichen planus: observations in 722 patients from India. J Oral Pathol, 1986: 15(2), 71-77.
7. Rybojad M, Moraillon I, Cordoliani F, et al. Lichen planus in the child: 25 cases. Clinical, follow-up and therapeutic aspects. Ann Dermatol Venereol, 2000, 127(6-7): 661.
8. Nanda A, Al-Ajmi HS, Al-Sabah H, et al. Childhood lichen planus: a report of 23 cases. Pediatr Dermatol, 2001, 18(10: 1-4.
9. Handa S, Sahoo B. Childhood lichen planus: a study of 87 cases. Int J Dermatol, 2002, 41(7): 423-427
10.吴志华.现代皮肤性病学,第1版,广州:广东人民出版社, 2000, 470-473.
11. Rymond L, Barnhill. Textbook of dermatopathology., 2nd ed. New York: McGraw-Hill.
12. Raghu AR, Nirmala NR, Sreekumaran N. Direct immunofluorescence in oral lichen planus and oral lichenoid reactions. Quintessence Int, 2002, 33(3): 234-239.
13. Mattsson T, Sundqvist KG, Heimdahl A, et al. A comparative immunological analysis of the oral mucosa in chronic graft-versus-host disease and oral lichen planus. Arch Oral Biol, 1992, 37(7): 539-547.
14. Shiohara T. The lichenoid tissue reaction. An immunological perspective. Am J Dermatopathol, 1988, 10(3): 252-256.
15. Sugerman PB, Satterwhite K, Bigby M. Autocytotoxic T-cell clones in lichen planus. Br J Dermatol, 2000, 142(3): 449-456.
16. Kawamura E, Nakamura S, Sasaki M, et al. Accumulation of oligoclonal T cells in the infiltrating lymphocytes in oral lichen planus. J Oral Pathol Med, 2003, 32(5): 282-289.
17. Sygerman PB, Savage NW, Walsh LJ, et al. The pathogenesis of oral lichen planus. Crit Rev Oral Biol Med, 2002, 13(4): 350-362.
18. Fayyazi A, Schweyer S, Soruri A, et al. T lymphocytes and altered keratinocytes express interferon-γand interleukin 6 in lichen planus. Arch Dermatol Res, 1999, 291(9): 485-490.
19. Villarroel Dorrego M, Correnti M, Delgado R, et al. Oral lichen planus: immunohistology of mucosal lesions. J Oral Pathol Med, 2002, 31(7): 410-414.
20. Khan A, Farah CS, Savage NW, et al. Th1 cytokines in oral lichen planus. J Oral Pathol Med, 2003, 32(2): 77-83.
21. Barker JN, Navsaria HA, Leiqh IM, et al. Gamma-interferon induced human keratinocyte HLA-DR synthesis: the role of dermal activated T-cells. Br J Dermatol, 1988, 119(5): 567-572.
22. Hasseus B, Jontell M, Brune M, et al. Langerhans cells and T cells in oral graft versus host disease and oral lichen planus. Scand J Immunol, 2001, 54(5): 516-524.
23. Dequchi M, Aiba S, Ohtani H , et al. Comparison of the distribution and numbers of antigen-presenting cells among T lymphocyte mediated dermatoses: CD1a+, factorⅫa+, and CD68+ cells in eczematous dermatitis, psoriasis, lichen planus and graft-versus-host disease. Arch Dermatol Res, 2002, 294(7): 297-302.
24. Zhao ZZ, Suqerman PB, Walsh LJ, et al. Exression of RANTES and CCR1 in oral lichen planus and association with mast cell migration. J Oral Pathol Med, 2002, 31(3): 158-162
25. Iijima W, Ohtani H, Nakayama T, et al. Infiltrting CD8+ T cells in oral lichen planus predominantly express CCR5 and CXCR3 and carry respective chemokine ligands RANTES/CCL5 and IP-10/CXCL10 in their cytolytic granules: a potential self-recruiting mechanism. Am J Pathol, 2003, 163(1): 261-268.
26. Little MC, Griffiths CE, Watson RE, et al. Oral mucosal keratinocytes express RANTES and ICAM-1, but not interleukin-8, in oral lichen planus and oral lichenoid reactions induced by amalgam fillings. Clin Exp Dermatol, 2003, 28(1): 64-69.
27. Zhao ZZ, Sugerman PB, Zhou XJ, et al. Mast cell degranulation and the role of T cell RANTES in oral lichen planus. Oral Dis, 2001, 7(4): 246-251.
28. Zhou XJ, Sugerman PB, Savage NW, et al. Intra-epithelial CD8+ T cells and basement membrane disruption in oral lichen planus. J Oral Pathol Med, 2002, 31(1): 23-27.
29. Zhou XJ, Sugerman PB, Savage NW, et al. Matrix metalloproteinases and their inhibitors in oral lichen planus. J Cutan Pathol, 2001, 28(2): 72-82.
30. Sandhu K, Handa S, Kanwar AJ. Familial lichen planus. Pediatr Dermatol, 2003, 20(2): 186.
31. Bermejo-Fenoll A, Lopez-Jornet P. Familial oral lichen planus: presentation of six families. Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 2006, 102(2): e12-15.
32. Kofoed ML, Lange Wantzin GL. Familial lichen planus-more frequent than previously suggested? J Am Acad Dermatol, 1985, 13(1): 50-54.
33. Graells J, Notario J, Badia F, et al. Lichen planus in monocygotic twins. Clin Exp Dermatol, 1998, 23(60: 299.
34. Ismail SB, Kumar SK, Zain RB. Oral lichen planus and lichenoid reactions:etiopathogenesis, diagnosis, management and malignant transformation. J Oral Sci, 2007, 49(2): 89-106.
35. Vallejo MJ, Huerta G, Cerero R, et al. Anxiety and depression as risk factors for oral lichen planus. Dermatology, 2001, 203(4), 303-307.
36. Eisen D. The clinical features, malignant potential, and systemic associations of oral lichen planus: a study of 723 patients. J Am Acad Dermatol, 2002, 46(2): 207-214.
37. Ivanovski K, Nakova M, Warburton G, et al. Psychological profile in oral lichen planus. J Clin Periodontol, 2005, 32(10): 1034-1040.
38.化红霞,白莉.扁平苔藓的病因及发病机制的研究进展.山西医药杂志, 2004, 33(10): 855-857.
39. Carrozzo M, Francia Di Celle P, Gandolfo S, et al. Increased frequency of HLA-DR6 allele in Italian patients with hepatitis C virus-associated oral lichen planus. Br J Dermatol, 2001, 144(4): 803-808.
40. Carrozzo M, Gandolfo S. Oral diseases possibly associated with hepatitis C virus. Crit Rev Oral Biol Med, 2003, 14(2): 115-127.
41. Lodi G, Giuliani M, Majorana A, et al. Lichen planus and hepatitis C virus: a multicentre study of patients with oral lesions and a systematic review. Br J Dermatol, 2004, 151(6): 1172-1181.
42. Lazaro P, Olalquiaqa J, Bartolome J, et al. Detection of hepatitis C virus RNA and core protein in keratinocytes form patients with cutaneous lichen planus and chronic hepatitis C. J Invest Dermatol, 2002, 11994): 798-803.
43. Kurokawa M, Hidaka T, Sasaki H, et al. Analysis of hepatitis C virus (HCV) RNA in the lesions of lichen planus in patients with chronic hepatitis C: detection of anti-genomic-as well as genomic-strand HCV RNAs in lichen planus lesions. J Dermatol Sci, 2003, 32(1): 65-70.
44. Eisen D. The clinical features, malignant potential, and systemic associations of oral lichen planus: a study of 723 patients. J Am Acad Dermatol, 2002, 46(2): 207-214.
45. Carrozzo M, Brancatello F, Dametto E, et al. Hepatitis C virus-associated oral lichen planus: is the geographical heterogeneity related to HLA-DR6? J Oral Pathol Med, 2005, 34(4): 204-208.
46. Nagao Y, Kawaquchi T, Ide T, et al. Exacerbation of oral erosive lichen planus by combination of interferon and ribavirin therapy for chronic hepatitis C. Int J Mol Med, 2005, 15(2): 237-241
47. Thivolet J, Viac J, Staquet MJ, et al. Cell-mediated immunity in wart infection. Int J Dermatol, 1982, 21(2): 94-98.
48. Chang F, Syrjanen S, Kellokoski J, et al. Human papillomavirus (HPV) infections and their associations with oral disease. J Oral Pathol Med, 1991, 20(7): 305-317.
49. OFlatharta C, Flint SR, Toner M, et al. Investigation into a possible association between oral lichen planus, the human herpesviruses, and the human papillomaviruses. Mol Diagn, 2003, 7(2): 73-83.
50. Dunsche A, Kastel A, Terheyden H, et al. Oral lichenoid reations associated with amalgam: improvement after amalgam removal. Br J Dermatol, 2003, 148(1): 70-76.
51. Dunsche A, Frank MP, Luttges J, et al. Lichenoid reactions of murine mucosa associated with amalgam. Br J Dermatol, 2003, 148(4): 741-748.
52. Wong L, Freeman S. Oral lichenoid lesions (OLL) and mercury in amalgam fillings. Contact Dermatitis, 2003, 48(2): 74-79.
53. Bagan JV, Thongprasom K, Scully C. Adverse oral reactions associated with the COX-2 inhibitor rofecoxib. Oral Dis, 2004, 10(6): 401-403
54. Scully C, Diz Dios P. Orofacial effects of antiretroviral therapies. Oral Dis, 2001, 7(4): 201-210
1. Brennan PA, Umar T, Palacios-Callender M, et al. A study to assess inducible nitric oxide synthase expression in oral lichen planus. J Oral Pathol Med, 2000, 29(6): 249-254.
2. Banchereau J, Briere F, Caux C, et al. Immunobiology of dendritic cells. Annu Rev Immunol, 2000, 18: 767-811
3. Banchereau J, Steinman RM. Dendritic cells and the control of immunity. Nature, 1998, 392(6673): 245-252.
4. Valladeau J, Ravel O, Dezutter-Dambuyant C, et al. Langerin, a novel C-type lectin specific to Langerhans cells, is an endocytic receptor that induces the formation of Birbeck granules. Immunity, 2000, 12(10: 71-81
5. Engering A, van Vliet SJ, Hebeda K, et al. Dynamic populations of dendritic cell-specific ICAM-3 grabbing nonintegrin-positive immature dendritic cells and liver/lymph node-specific ICAM-3 grabbing nonintegrin-positive endothelial cells in the outer zones of the paracortex of human lymph nodes. Am J Pathol, 2004, 164(5): 1587-1595
6. Albert ML. Death-defying immunity: do apoptotic cells influence antigen processing and presentation? Nat Rev Immunol, 2004, 493): 223-231.
7. Santoro A, Majorana A, Roversi L, et al. Recruitment of dendritic cells in oral lichen planus. J Pathol, 2005, 205(4), 426-434.
8. Kadowaki N, Antonenko S, Lau JY, et al. Natural interferon alpha/beta-producing cells link innate and adaptive immunity. J Exp Med, 2000, 192(2): 219-226.
9. Kirou KA, Vakkalanka RK, Butler MJ, et al. Induction of Fas ligand-mediated apoptosis by interferon-alpha. Clin Immunol, 2000, 95(3): 218-226
10. Christofidou-Solomidou M, Albelda SM, et al. Experimental production and modulation of human cytotoxic dermatitis in human-murine chimeras. Am J Pathol, 1997, 150(2): 631-639.
11. Sugerman PB, Savage NW, Xu LJ, et al. Heat shock protein expression in oral lichen planus. J Oral Pathol Med, 1995, 24(1): 1-8.
12. Younqnak-Piboonratanakit P, Tsushima F, Otsuki n, et al. The expression of B7-H1 on keratinocytes in chronic inflammatory mucocutaneous disease and its regulatory role. Immunol Lett, 2004, 94(3): 215-222.
13. Walsh LJ. Mast cells and oral inflammation. Crit Rev Oral Biol Med, 2003, 14(3):188-198.
14. Zhou XJ, Sugerman PB, Savage NW, et al. Intra-epithelial CD8+ T cells and basement membrane disruption in oral lichen planus. J Oral Pathol Med, 2002, 31(1): 23-27.
15.樊娟丽,白莉.扁平苔藓免疫学研究进展.中国麻风皮肤病杂志, 2005, 21(12):967-969.
16. Khan A, Farah CS, Savage NW, et al. Th1 cytokines in oral lichen planus. J Oral Pathol Med, 2003, 32(2): 77-83.
17. Suqerman PB, Savage NW, Zhou X, et al. Oral lichen planus, Clin Dermatol, 2000, 18(5): 533-539.
18. Simark-Mattsson C, Berqenholtz G, Jontell M, et al. Distribution of interleukin-2, -4, -10, tumour necrosis factor-alpha and transforming growth factor-beta mRNAs in oral lichen planus. Arch Oral Biol, 1999, 44(6): 499-507.
19. Sugerman PB, Savage NW, Seymour GJ, et al. Is there a role for tumour necrosis factor alpha (TNF-alpha) in oral lichen planus? J Oral Pathol Med, 1996, 25(5): 219-224.
20. Sugerman PB, Satterwhite K, Bigby M. Autocytotoxic T-cell clones in lichen planus. Br J Dermatol, 2000, 142(3): 449-456
21. Rich AM, Reade PC. A quantitative assessment of Langerhans cells in oral mucosal lichen planus and leukoplakia. Br J Dermatol, 1989, 120(2): 223-228.
22. Farthing PM, Matear P, Cruchley AT. The activation of Langerhans cells in oral lichen planus. J Oral Pathol Med, 1990, 19(2): 81-85.
23. Albanesi C, Cavani A, Girolomoni G. Interferon-gamma-stimulated human keratinocytes express the genes necessary for the production of peptide-loaded MHC classⅡmolecules. J Invest Dermatol, 1998, 110(2): 138-142.
24. Zhao ZZ, Savage NW, Sugermann PB, et al. Mast cell/T cell interactions in oral lichen planus. J Oral Pathol Med. 2002, 31(4): 189-195.
25. Sistig S, Vucicevic-Boras V, Lukac J, et al. Salivary IgA and IgG subclasses in oral mucosal diseases. Oral Dis, 2002, 8(6): 282-286.
26. Lukac J, Brozovic S, Vucicevic-Boras V, et al. Serum autoantibodies to desmogleins 1 and 3 in patients with oral lichen planus. Croat Med J, 2006, 47(1): 53-58.
27.张学军.皮肤性病学.第5版.北京:人民卫生出版社, 13-15.
28. Simark-Mattsson C, Jontell M, Bergenholtz G, et al. Distribution of interferon-gamma mRNA-positive cells in oral lichen planus lesions. J Oral Pathol Med, 1998, 27(10): 483-488.
29. Simark-Mattsson C, Berqenholtz G, Jontell M, et al. Distribution of interleukin-2, -4, -10, tumour necrosis factor-alpha and transforming growth factor-beta mRNA in oral lichen planus. Arch Oral Biol, 1999, 44(6): 499-507.]
30. Sigidin YA, Loukina GV, Skurkovich B, et al. Randomized, double-blind trial of anti-interferon-gamma antibodies in rheumatoid arthritis. Scand J Rheumatol, 2001, 30(4): 203-207.
31. Leung BP, McInnes IB, Esfandiari E, et al. Combined effects of IL-12 and IL-18 on the induction of collagen-induced arthritis. J Immunol, 2000, 164(12): 6495-6502.
32. Costa GL, Sandora MR, Nakajima A, et al. Adoptive immunotherapy of experimental autoimmune encephalomyelitis via T cell delivery of the IL-12 p40 subunit. J Immunol, 2001, 167(4): 2379-2387.
33. Spandau U, Toksoy A, Goebeler M, et al. MIG is a dominant lymphocyte-attractant chemokine in lichen planus lesions. J Invest Dermatol, 1998, 111(6): 1003-1009.
34. Toruniowa B, Krasowska D, Koziol M, et al. Serum levels of IL-6 in mycosis fungoides, psoriasis and lichen planus. Ann N Y Acad Sci, 1995, 762: 432-434.
35. Toruniowa B, Krasowska D, Koziol M, et al. Serum levels of IL-6 in mycosis fungoides, psoriasis and lichen planus. Ann N Y Acad Sci, 1995, 762: 432-434.
36. Yamamoto T, Yoneda K, Ueta E, et al. Serum cytokines, interleukin-2 receptor, and soluble intercellular adhesion molecule-1 in oral disorders. Oral Surg Oral Med Oral Pathol, 1994, 78(6): 727-735.
37. Sun A, Chia JS, Chang YF, et al. Serum interleukin-6 level is a useful marker inevaluating therapeutic effects of levamisole and Chinese medicinal herbs on patients with oral lichen planus. J Oral Pathol Med, 2002, 31(4): 196-203.
38. Chen F, Castranova V, Shi X. New insights into the role of nuclear factor-kappa B in cell growth regulation. Am J Pathol, 2001, 159(2): 387-397
39. Bours V, Bonizzi G, Bentires-Alj M, et al. NF-kappaB activation in response to toxical and therapeutical agents: role in inflammation and cancer treatment. Toxicology, 2000, 153(1-3): 27-38.
40. Li Q, Verma IM. NF-kappaB regulation in the immune system. Nat Rev Immunol, 2002, 2(10): 725-734.
41. Wan YY, DeGregori J. The survival of antigen-stimulated T cells requires NF kappaB-mediatd inhibition of p73 expression. Immunity, 2003, 18(3): 331-342.
42. Khan A, Farah CS, Savage NW, et al. Th1 cytokines in oral lichen planus. J Oral Pathol Med, 2003, 32(2): 77-83.
43. Sklavounous A, Chrysomali E, Scorilas A, et al. TNF-alpha expression and apoptosis-regulating proteins in oral lichen planus: a comparative immunohistochemical evaluation. J Oral Pathol. Med, 2000, 29(8): 370-375.
44. Sun A, Chia JS, Chang YF, et al. Serum interleukin-6 level is a useful marker in evaluating therapeutic effects of levamisole and Chinese medicinal herbs on patients with oral lichen planus. J Oral Pathol Med, 2002, 31(4): 196-203
45. Santoro A, Majorana A, Bardellini E, et al. NF-kappaB expression in oral and cutaneous lichen planus. J Pathol, 2003, 201(3): 466-472.
46. Pezelj-Ribaric S, Prso IB, Abram M, et al. Salivary levels of tumor necrosis factor-alpha in oral lichen planus. Med inflamm, 2004, 1392): 131-133.
2王椿森,李家文,等.皮肤性病免疫学.武汉:湖北科学技术出版社, 1999, 229-234.
3 Sugerman PB, Savage NW, Walsh LJ, et al. The pathogenesis of oral lichen planus. Crit Rev Oral Biol Med, 2002, 13(4): 350-365.
4 Walsh LJ, Savage NW, Ishii T, et al. Immunopathogenesis of oral lichen planus. J Oral pathol Med, 1990, 19(9): 389-396.
5赵辩.临床皮肤病学,第3版,南京:江苏科学技术出版社, 2001, 782-789
6 Bascones-Ilundain C, Gonzalez-Moles MA, Esparza-Gomez G, et al. Importance of apoptotic mechanisms in inflammatory infiltrate of oral lichen planus lesions. Anticancer Res, 2006, 26(1A): 357-362.
7 Weedon D, Searle J, Kerr JF. Apoptosis. Its nature and implications for dermatopathology. Am J dermatopathol, 1979, 1(2): 133-144.
8 Bloor BK, Malik FK, Odell EW, et al. Quantitative assessment of apoptosis in oral lichen planus, Oral Surg Oral Med Oral Pathol Radiol Endod, 1999, 88(2): 187-195.
9 Tobon-Arroyaye SI, Villegas-Acosta FA, Ruiz-Restrepo SM, et al. Expression of caspase-3 and structural changes associated with apoptotic cell death of keratincytes in oral lichen planus. Oral Dis, 2004, 10(3): 173-178.
10李鑫,丁政云,刘丽娟. 35例扁平苔藓临床和组织病理分析.中国麻风皮肤病杂志, 2007, 23(8): 686-687
11 Kyriakis KP, Terzoudi S, Palamaras I, et al. Sex and age distribution of patients with lichen planus. J Eur Acad Dermatol Venereol, 2006, 20(5): 302-626.
12吴志华.现代皮肤性病学,第1版,广州:广东人民出版社, 2000, 470-473.
1 Thornhill MH. Immune mechanisms in oral lichen planus. Acta Odontol Scand, 2001, 59(3): 174-177.
2 Dissemond J, Schroter S, Franckson T, et al. Pimecrolimus in an adhesive ointment as a new treatment option for oral lichen planus. Br J Dermatol, 2004, 150(4): 782-784.
3朱学骏、涂平.皮肤病的组织病理诊断.第2版.北京:北京医科大学出版社, 2001. 138.
4 Prpic Masssari L, Kastelan M, Cruber F, et al. Perforin expression in peripheral blood lymphocytes and skin-infiltrating cells in patients with lichen planus. Br J Dermatol, 2004; 151(2): 433-439
5 Sklavounou A, Chrysomali E, Scorilas A, et al. TNF-alpha expression and apoptosis-regulating proteins in oral lichen planus: a comparative immunohistochemical evaluation. J Oral Pathol Med, 2000, 29(8): 370-375.
6苏有明,于民,阎锋,等.限局性硬皮病血清sIL-2R、TNF-α水平和T淋巴细胞亚群的检测.临床皮肤科杂志, 1998, 27: 8-10.
7聂本勇,郑茂荣,范表源. TNF-α和IL-1β对HaCaT细胞诱生型一氧化氮合酶表达的影响.中国皮肤性病学杂志, 2004, 18: 68-70.
8陈建粮.细胞间粘附分子1表达的调控.国外医学免疫学分册, 2000, 23: 272-274.
9李红文,丁一,邓新国,等. ICAM-1、IGF-1在银屑病皮损中的表达.中国皮肤性病学杂志, 2001, 15: 297-298.
10狄正鸿,许静.扁平苔藓皮损中浸润淋巴细胞的研究.中国医科大学学报, 2006,35(4): 427-428.
11 Iijima W, Ohtani H, Nakayama T, et al. Infliltrating CD8+ T cells in oral lichen planus predominantly express CCR5 and CXCR3 and carry respective chemokine ligands RANTES/CCL5 and IP-10/CXCL10 in their cytolytic granules: a potential self -recruiting mechanism. Am J Pathol, 2003, 163(1): 261-268.
12 al-Janadi M, al-Balla S, al-Dalaan A, et al. Cytokine profile in systemic lupus erythematosus, rheumatoid arthritis, and other rheumatic diseases. J Clin Immunol, 1993, 13(1): 58-67.
13 Kono T, Tanii T, Furukawa M, et al. Effects of human recombinant tumor necrosis factor-alpha (TNF-alpha) on the proliferative potential of human keratinocytes cultured in serum-free medium. J Dermatol, 1990, 17(7): 409-413.
14 Farrell AM, Dean D, Millard PR, et al. Cytokine alterations in lichen sclerosus: an immunohistochemical study. Br J Dermatol, 2006, 155(5): 931-940.
15 Sugerman PB, Savage NW, Zhou X, et al. Oral lichen planus. Clin Dermatol, 2000, 18(5): 533-539.
16 Johansen C, Funding AT, Otkjaer K, et al. Protein expression of TNF-alpha in psoriatic skin is regulated at a posttranscriptional level by MAPK-activated protein kinase 2. J Immunol, 2006, 176(3): 1431-1438.
17 Sklavounou A, Chrysomali E, Scorilas A, et al. TNF-alpha expression and apoptosis-regulating proteins in oral lichen planus; a comparative immunohistochemical evaluation. J Oral Pathol Med, 2000, 29(8): 370-375.
18陈莉芬,李荣亨.肿瘤坏死因子α在肾脏疾病中的研究进展.国外医学泌尿系统分册, 2001, 21(4):147-149.
19 Beamer NB, Coull BM, Clark WM, et al. Interleukin-6 and interleukin-1 receptor antagonist in acute stroke. Ann Neurol, 1995, 37(6): 800-805.
20 Fassbender K, Rossol S, Kammer T, et al. Proinflammatory cytokines in serum of patients with acute cerebral ischemia: kinetics of sectetion and relation to the extent ofbrain damage and outcome of disease. J Neurol Sci, 1994, 122(2): 135-139.
21 Diamond MS, Staunton DE, Marlin SD, et al. Binding of the integrin Mac-1 (CD11b/CD18) to the third immunoglobulin-like domain of ICAM-1 (CD54) and its regulation by glycosylation. Cell, 1991, 65(6): 961-971.
22 Marlin SD, Stauton DE, Springer TA, et al. A soluble form of intercellular adhesion molecule-1 inhibits rhinovirus infection. Nature, 1990, 344(6261): 70-72.
23于新波,杨丕山.细胞间粘附分子-1在牙周炎中作用的研究现状.国外医学口腔医学分册, 2002, 29(6): 340-342.
24 Hagi-Pavli E, Farthing PM, Henshaw FN, et al. Presentation of ICAM-1 protein at the cell surface of oral keratinocytes in the presence of adrenomedullin and corticotrophin. Cell Physiol Biochem, 2005, 15(1-4): 167-174.
25 Carrozzo M, Uboldi de Capei M, Dametto E, et al. Tumor necrosis factor-alpha and interferon-gamma polymorphisms contribute to susceptibility to oral lichen planus. J Invest Dermatol, 2004, 122(1): 87-94.
1 Earnshaw WC, Martins LM, Kaufmann SH, et al. Mammalian caspase: structure, activation, substrates, and functions during apoptosis. Annu Rev Biochem, 1999, 68: 383-424.
2 Ferrer I, Planas AM. Signaling of cell death and cell survival following focal cerebral ischemia: life and death struggle in the penumbra. J Neuropathol Exp Neurol, 2003, 62(4): 329-339.
3 Zhang F, Yin W, Chen J. Apoptosis in cerebral ischemia: executional and regulatory signaling mechanisms. Neurol Res, 2004, 26(8): 835-845.
4 Plesnila N, Zhu C, Culmsee C, et al. Nuclear translocation of apoptosis-inducing factor after focal cerebral ischemia. J Cereb Blood Flow Metab, 2004, 24(4): 458-466.
5 Dekker NP, Lozada-Nur F, Lagenaur LA, et al. Apoptosis associated markers in orallichen planus. J Oral Pathol Med, 1997, 26(4): 170-175.
6 Neppelberg E, Johannessen AC, Jonsson R. Apoptosis in oral lichen planus. Eur J Oral Sci, 2001, 109(5): 361-364.
7 Li MH, Ito D, Sanada M, et al. Effect of 5-fluorouracil on G1 phase cell cycle regulation in oral cancer cell lines. Oral Oncol, 2004, 40(1): 63-70.
8 Villarroel Dorrego M, Correnti M, et al. Oral lichen planus: immunohistology of mucosal lesions. J Oral Pathol Med, 2002, 31(7): 410-414.
9 Bascones C, Gonzalez-Moles MA, Esparza G, et al. Apoptosis and cell cycle arrest in oral lichen planus Hypothesis on their possible influence on its malignant transformation. Arch Oral Biol, 2005, 50(10): 873-881.
10 Kerr JF, Wyllie AH, Currie AR. Apoptosis: a basic biological phenomenon with wide-rageing implication in tissue kenetics. Br J Cancer, 1972, 26(4): 239-257.
11 Suzuki A, Iwsaki M, Wagai N, et al. Involvement of cytoplasmic serine proteinase and CPP32 subfamily in the molecular machinery of Caspase-3 activiation during Fas-mediated apoptosis. Exp Cell Res, 1997, 233(1): 48-55.
12 Nicholson DW, Ali A, Thornberry NA, et al Identification and inhibition of the ICE/CED-3 protease necessary for mammalian apoptosis. Nature, 1995, 376(6535): 37-43.
13 Saikumar P, Dong Z, Mikhailov V, et al. Apoptosis: definition, mechanism, and relevance to disease. Am J Med, 1999, 107(5): 489-506.
14 Roy S, Bayly CI, Gareau Y, et al. Maintenance of caspase-3 proenzyme dormancy by an intrinsic“safety catch”regulatory tripeptide. Proc Natl Acad Sci USA, 2001, 98(11): 6132-6137.
15 Sklavounou A, Chrysomali E, Scorilas A, et al. TNF-alpha expression and apoptosis-regulating proteins in oral lichen planus: a comparative immunohistochemical evaluation. J Oral Pathol Med, 2000, 29(8): 370-375.
16 Khan A, Farah CS, Savage NW, et al. Th1 cytokines in oral lichen planus. J OralPathol Med, 2003, 32(2): 77-83.
17 Sugerman PB, Savage NW, Zhou X, et al. Oral lichen planus, Clin Dermatol, 2000, 18: 533-539.
18 Tobon-Arroyave SI, Villegas-Acosta FA, Ruiz-Restrepo SM, et al. Expression of caspase-3 and structural changes associated with apoptotic cell death of keratinocytes in oral lichen planus. Oral Dis, 2004, 10(3): 173-178.
19 Nicholson DW, Thornberry NA. Apoptosis. Life and death decisions. Science, 2003, 299(6504): 214-215.
20陈彦灵,童坦君.细胞凋亡是半胱天冬酶参与的复杂过程.生命科学, 2000, 20(2): 77-79.
21 Luo C, Zhu C, Jiang J, et al. Alterations of bcl-2, bcl-x and bax protein expressions in area CA-3 of rat hippocampus following fluid percussion brain injury. Chin J Traumatol, 1999, 2(2): 101-104.
22 Oltvai ZN, Mlilliman CL, Korsmeyer SJ. Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death. Cell, 1993, 74(4); 609-619.
23 Borner C. The Bcl-2 protein family: sensors and checkpoints for life-or-death decisions. Mol Immunol, 2003, 39(11): 615-647.
24孙红,惠延年,王立勤,等. Caspase-3和bax在视网膜母细胞瘤中的表达.第四军医大学学报2003; 24: 1162-1163
1 Dekker NP, Lozada-Nur F, Lagenaur LA, et al. Apoptosis-associated markers in oral lichen planus. J Oral Pathol Med, 1997, 26(4): 170-175.
2 Neppelberg E, Johannessen AC, Jonsson R. Apoptosis in oral lichen planus. Eur J Oral Sci, 2001, 109(5): 361-364
3 Walsh LJ, Savage NW, Ishii T, et al. Immunopathogenesis of oral lichen planus. J Oral Pathol Med, 1990, 19(9): 389-396.
4 Majorana A, Facchetti F, Pellegrini W, et al. Apoptosis-associated markers in oral lichen planus. J Oral Pathol Med, 1999, 28(1): 47-48.
5 Li MH, Ito D, Sanada M, et al. Effect of 5-fluorouracil on G1 phase cell cycle regulation in oral cancer cell lines. Oral Oncol, 2004, 40(1): 63-70.
6 Bloor BK, Malik FK, Odell EW, et al. Quantitative assessment of apoptosis in oral lichen planus, Oral Surg Oral Med Oral Pathol Radiol Endod, 1999, 88(2): 187-195.
7 Tobon-Arroyave SI, Villegas-Acosta FA, Ruiz-Restrepo SM, et al. Expression of caspase-3 and structural changes associated with apoptotic cell death of keratincytes in oral lichen planus. Oral Dis, 2004, 10(3): 173-178.
8 Motokura T, Bloom T, Kim HG, et al. A novel cyclin encoded by a bcl1-linked candidate oncogene. Nature, 1991, 350(6318): 512-515.
9 Xiong Y, Connolly T, Futcher B, et al. Human D-type cyclin. Cell, 1991, 65(4): 691-699.
10 Hunter T, Pines J. Cyclins and cancer II: Cyclin D and CDK inhibitors come of age. Cell, 1994, 79(4): 573-582.
11 Sherr CJ. G1 phase progression: Cycling on cue. Cell, 1994, 79(4): 551-555.
12 Gonzalez-Moles MA, Bascones-Ilundain C, Gil Montoya JA, et al. Cell cycle regulation mechanisms in oral lichen planus: molecular bases in epithelium predisposed to malignant transformation. Arch Oral Biol, 2006, 51(12): 1093-1103.
13 Tipoe GL, Jin V, White FH. The relationship between vascularity and cell proliferation in human normal and pathological lesions of the oral cheek epithelium. Eur J Cancer B Oral Oncol, 1996: 32B(1), 24-31.
14 Acay RR, Felizzola CR, de Araujo N, et al. Evaluation of proliferative potential in oral lichen planus and oral lichenoid lesions using immunohistochemical expression of p53 and Ki67. Oral Oncol, 2006, 42(5): 475-480.
15王业东,王林杰,王松山,等.慢性肝炎和原发性肝癌肝组织P21和P15蛋白的表达及与细胞凋亡的关系.中华实验和临床病毒学杂志, 2000, 14(2): 157-159.
16 Bascones C, Gonzalez-Moles MA, Esparza G, et al. Apoptosis and cell cycle arrest in oral lichen planus Hypothesis on their possible influence on its malignant transformation. Archives of Oral Biology, 2005, 50(10): 873-881.
1.陈敬,董德琼,杨渝浩.白介素-12与结核病.国外医学呼吸系统分册, 2002, 22(4): 220-222.
2. Simark-Mattsson C, Jontell M, Bergenholtz G, et al. Distribution of interferon-gamma mRNA-positive cells in oral lichen planus lesions. J Oral Pathol Med, 1998, 27(10): 483-488.
3. Simark-Mattsson C, Bergenholtz G, Jontell M, et al. Distribution of interleukin-2, -4, -10, tumour necrosis factor-alpha and transforming growth factor-beta mRNA in oral lichen planus. Arch Oral Biol, 1999, 44(6): 499-507.
4.郭海建,刘断民,刘俊,等.溃疡性结肠炎患者PBMC体外白细胞介素12诱生水平研究.实用临床医药杂志, 2007, 11(5): 65-67
5.吴雄文,梁智辉.实用免疫学实验技术,第1版,武汉:湖北科学技术出版社, 2002, 124-125.
6.唐皓,马中富.白介素-12的研究新进展.国外医学临床生物化学与检验学分册, 2001, 22(4): 177-178.
7. Trinchieri G. Interleukin-12 and the regulation of innate resistance and adaptive immunity. Nat Rev Immunol, 2003, 3(2): 133-146.
8. Schakel K, von Kietzell M, Hansel A, et al. Human 6-Sulfo LacNAc-expressing dendritic cells are principal producers of early interleukin-12 and are controlled by erythrocytes. Immunity, 2006, 24(6): 767-777.
9. Huang Q, Liu D, Majewski P, et al. The plasticity of dendritic cell responses to pathogens and their components. Science, 2001, 294(5543): 870-875.
10. Yu Y, Tang L, Wang J, et al. Psoriatic lesional keratinocytes promote the maturation of human monocyte-derived Langerhans cells. Dermatology, 2002, 204(2): 94-99.
11. Leung BP, McInnes IB, Esfandiari E, et al. Combined effects of IL-12 and IL-18 on the induction of collagen-induced arthritis. J Immunol, 2000, 164(12): 6495-6502.
12. Yano S, Komine M, Fujimoto M, et al. Interleukin 15 induces the signals of epidermal proliferation through ERK and PI3-kinase in a human epidermal keratinocyte cell line, HaCaT. Biochem Biophys Res Commun, 2003, 301(4): 841-847.
13.徐钰,高占成.白介素-12在支气管哮喘中的作用机制.国外医学呼吸系统分册, 2002, 22(6): 289-296.
14. Wenzel J, Scheler M, Proelss J et al. TypeⅠinterferon-associated cytotoxic inflammation in lichen planus. J Cutan Pathol, 2006, 33(1): 672-678.
15. Nestle FO, Conrad C. The IL-12 family member p40 chain as a master switch and novel therapeutic target in psoriasis. J Invest Dermatol, 2004, 123(6): xiv-xv.
16.狄正鸿,许静.扁平苔藓皮损中浸润淋巴细胞的研究.中国医科大学学报, 2006, 35(4): 427-428.
17. Simark-Mattsson C, Jontell M, Bergenholtz G, et al. Distribution of interferon-gamma mRNA-positive cells in oral lichen planus lesions. J Oral Pathol Med, 1998, 27(10): 483-488.
18. Simark-Mattsson C, Bergenholtz G, Jontell M, et al. Distribution of interleukin-2, -4, -10, tumour necrosis factor-alpha and transforming growth factor-beta mRNA in oral lichen planus. Arch Oral Biol, 1999, 44(6): 499-507.
1. Kyriakis KP, Terzoudi S, Palamaras I, et al. Sex and age distribution of patients with lichen planus. J Eur Acad Dermatol Venereol, 2006, 20(5): 302-626.
2. Calnan CD, Meara RH. St John’s Hospital diagnostic index. Trans Rep St John’s Hosp Derm Soc Lond, 1957, 39: 56-68
3. Depaoli M. Lichen rubber planus, clinical and statistical features. Minerva Dermatol, 1964, 39: 166-171.
4. Schmidt H. Frequency, duration and localization of lichen planus. A study based on 181 patients. Acta Derm Venereol, 1961, 41: 164-167.
5. Ikeda N, Ishii T, Iida S, et al. Epidemiological study of oral leukoplakia based on mass screening for oral mucosal diseases in a selected Japanese population. Community Dent Oral Epidemiol, 1991, 19(3): 160-163.
6. Murti PR, Daftary DK, Bhonsle RB, et al. Malignant potential of oral lichen planus: observations in 722 patients from India. J Oral Pathol, 1986: 15(2), 71-77.
7. Rybojad M, Moraillon I, Cordoliani F, et al. Lichen planus in the child: 25 cases. Clinical, follow-up and therapeutic aspects. Ann Dermatol Venereol, 2000, 127(6-7): 661.
8. Nanda A, Al-Ajmi HS, Al-Sabah H, et al. Childhood lichen planus: a report of 23 cases. Pediatr Dermatol, 2001, 18(10: 1-4.
9. Handa S, Sahoo B. Childhood lichen planus: a study of 87 cases. Int J Dermatol, 2002, 41(7): 423-427
10.吴志华.现代皮肤性病学,第1版,广州:广东人民出版社, 2000, 470-473.
11. Rymond L, Barnhill. Textbook of dermatopathology., 2nd ed. New York: McGraw-Hill.
12. Raghu AR, Nirmala NR, Sreekumaran N. Direct immunofluorescence in oral lichen planus and oral lichenoid reactions. Quintessence Int, 2002, 33(3): 234-239.
13. Mattsson T, Sundqvist KG, Heimdahl A, et al. A comparative immunological analysis of the oral mucosa in chronic graft-versus-host disease and oral lichen planus. Arch Oral Biol, 1992, 37(7): 539-547.
14. Shiohara T. The lichenoid tissue reaction. An immunological perspective. Am J Dermatopathol, 1988, 10(3): 252-256.
15. Sugerman PB, Satterwhite K, Bigby M. Autocytotoxic T-cell clones in lichen planus. Br J Dermatol, 2000, 142(3): 449-456.
16. Kawamura E, Nakamura S, Sasaki M, et al. Accumulation of oligoclonal T cells in the infiltrating lymphocytes in oral lichen planus. J Oral Pathol Med, 2003, 32(5): 282-289.
17. Sygerman PB, Savage NW, Walsh LJ, et al. The pathogenesis of oral lichen planus. Crit Rev Oral Biol Med, 2002, 13(4): 350-362.
18. Fayyazi A, Schweyer S, Soruri A, et al. T lymphocytes and altered keratinocytes express interferon-γand interleukin 6 in lichen planus. Arch Dermatol Res, 1999, 291(9): 485-490.
19. Villarroel Dorrego M, Correnti M, Delgado R, et al. Oral lichen planus: immunohistology of mucosal lesions. J Oral Pathol Med, 2002, 31(7): 410-414.
20. Khan A, Farah CS, Savage NW, et al. Th1 cytokines in oral lichen planus. J Oral Pathol Med, 2003, 32(2): 77-83.
21. Barker JN, Navsaria HA, Leiqh IM, et al. Gamma-interferon induced human keratinocyte HLA-DR synthesis: the role of dermal activated T-cells. Br J Dermatol, 1988, 119(5): 567-572.
22. Hasseus B, Jontell M, Brune M, et al. Langerhans cells and T cells in oral graft versus host disease and oral lichen planus. Scand J Immunol, 2001, 54(5): 516-524.
23. Dequchi M, Aiba S, Ohtani H , et al. Comparison of the distribution and numbers of antigen-presenting cells among T lymphocyte mediated dermatoses: CD1a+, factorⅫa+, and CD68+ cells in eczematous dermatitis, psoriasis, lichen planus and graft-versus-host disease. Arch Dermatol Res, 2002, 294(7): 297-302.
24. Zhao ZZ, Suqerman PB, Walsh LJ, et al. Exression of RANTES and CCR1 in oral lichen planus and association with mast cell migration. J Oral Pathol Med, 2002, 31(3): 158-162
25. Iijima W, Ohtani H, Nakayama T, et al. Infiltrting CD8+ T cells in oral lichen planus predominantly express CCR5 and CXCR3 and carry respective chemokine ligands RANTES/CCL5 and IP-10/CXCL10 in their cytolytic granules: a potential self-recruiting mechanism. Am J Pathol, 2003, 163(1): 261-268.
26. Little MC, Griffiths CE, Watson RE, et al. Oral mucosal keratinocytes express RANTES and ICAM-1, but not interleukin-8, in oral lichen planus and oral lichenoid reactions induced by amalgam fillings. Clin Exp Dermatol, 2003, 28(1): 64-69.
27. Zhao ZZ, Sugerman PB, Zhou XJ, et al. Mast cell degranulation and the role of T cell RANTES in oral lichen planus. Oral Dis, 2001, 7(4): 246-251.
28. Zhou XJ, Sugerman PB, Savage NW, et al. Intra-epithelial CD8+ T cells and basement membrane disruption in oral lichen planus. J Oral Pathol Med, 2002, 31(1): 23-27.
29. Zhou XJ, Sugerman PB, Savage NW, et al. Matrix metalloproteinases and their inhibitors in oral lichen planus. J Cutan Pathol, 2001, 28(2): 72-82.
30. Sandhu K, Handa S, Kanwar AJ. Familial lichen planus. Pediatr Dermatol, 2003, 20(2): 186.
31. Bermejo-Fenoll A, Lopez-Jornet P. Familial oral lichen planus: presentation of six families. Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 2006, 102(2): e12-15.
32. Kofoed ML, Lange Wantzin GL. Familial lichen planus-more frequent than previously suggested? J Am Acad Dermatol, 1985, 13(1): 50-54.
33. Graells J, Notario J, Badia F, et al. Lichen planus in monocygotic twins. Clin Exp Dermatol, 1998, 23(60: 299.
34. Ismail SB, Kumar SK, Zain RB. Oral lichen planus and lichenoid reactions:etiopathogenesis, diagnosis, management and malignant transformation. J Oral Sci, 2007, 49(2): 89-106.
35. Vallejo MJ, Huerta G, Cerero R, et al. Anxiety and depression as risk factors for oral lichen planus. Dermatology, 2001, 203(4), 303-307.
36. Eisen D. The clinical features, malignant potential, and systemic associations of oral lichen planus: a study of 723 patients. J Am Acad Dermatol, 2002, 46(2): 207-214.
37. Ivanovski K, Nakova M, Warburton G, et al. Psychological profile in oral lichen planus. J Clin Periodontol, 2005, 32(10): 1034-1040.
38.化红霞,白莉.扁平苔藓的病因及发病机制的研究进展.山西医药杂志, 2004, 33(10): 855-857.
39. Carrozzo M, Francia Di Celle P, Gandolfo S, et al. Increased frequency of HLA-DR6 allele in Italian patients with hepatitis C virus-associated oral lichen planus. Br J Dermatol, 2001, 144(4): 803-808.
40. Carrozzo M, Gandolfo S. Oral diseases possibly associated with hepatitis C virus. Crit Rev Oral Biol Med, 2003, 14(2): 115-127.
41. Lodi G, Giuliani M, Majorana A, et al. Lichen planus and hepatitis C virus: a multicentre study of patients with oral lesions and a systematic review. Br J Dermatol, 2004, 151(6): 1172-1181.
42. Lazaro P, Olalquiaqa J, Bartolome J, et al. Detection of hepatitis C virus RNA and core protein in keratinocytes form patients with cutaneous lichen planus and chronic hepatitis C. J Invest Dermatol, 2002, 11994): 798-803.
43. Kurokawa M, Hidaka T, Sasaki H, et al. Analysis of hepatitis C virus (HCV) RNA in the lesions of lichen planus in patients with chronic hepatitis C: detection of anti-genomic-as well as genomic-strand HCV RNAs in lichen planus lesions. J Dermatol Sci, 2003, 32(1): 65-70.
44. Eisen D. The clinical features, malignant potential, and systemic associations of oral lichen planus: a study of 723 patients. J Am Acad Dermatol, 2002, 46(2): 207-214.
45. Carrozzo M, Brancatello F, Dametto E, et al. Hepatitis C virus-associated oral lichen planus: is the geographical heterogeneity related to HLA-DR6? J Oral Pathol Med, 2005, 34(4): 204-208.
46. Nagao Y, Kawaquchi T, Ide T, et al. Exacerbation of oral erosive lichen planus by combination of interferon and ribavirin therapy for chronic hepatitis C. Int J Mol Med, 2005, 15(2): 237-241
47. Thivolet J, Viac J, Staquet MJ, et al. Cell-mediated immunity in wart infection. Int J Dermatol, 1982, 21(2): 94-98.
48. Chang F, Syrjanen S, Kellokoski J, et al. Human papillomavirus (HPV) infections and their associations with oral disease. J Oral Pathol Med, 1991, 20(7): 305-317.
49. OFlatharta C, Flint SR, Toner M, et al. Investigation into a possible association between oral lichen planus, the human herpesviruses, and the human papillomaviruses. Mol Diagn, 2003, 7(2): 73-83.
50. Dunsche A, Kastel A, Terheyden H, et al. Oral lichenoid reations associated with amalgam: improvement after amalgam removal. Br J Dermatol, 2003, 148(1): 70-76.
51. Dunsche A, Frank MP, Luttges J, et al. Lichenoid reactions of murine mucosa associated with amalgam. Br J Dermatol, 2003, 148(4): 741-748.
52. Wong L, Freeman S. Oral lichenoid lesions (OLL) and mercury in amalgam fillings. Contact Dermatitis, 2003, 48(2): 74-79.
53. Bagan JV, Thongprasom K, Scully C. Adverse oral reactions associated with the COX-2 inhibitor rofecoxib. Oral Dis, 2004, 10(6): 401-403
54. Scully C, Diz Dios P. Orofacial effects of antiretroviral therapies. Oral Dis, 2001, 7(4): 201-210
1. Brennan PA, Umar T, Palacios-Callender M, et al. A study to assess inducible nitric oxide synthase expression in oral lichen planus. J Oral Pathol Med, 2000, 29(6): 249-254.
2. Banchereau J, Briere F, Caux C, et al. Immunobiology of dendritic cells. Annu Rev Immunol, 2000, 18: 767-811
3. Banchereau J, Steinman RM. Dendritic cells and the control of immunity. Nature, 1998, 392(6673): 245-252.
4. Valladeau J, Ravel O, Dezutter-Dambuyant C, et al. Langerin, a novel C-type lectin specific to Langerhans cells, is an endocytic receptor that induces the formation of Birbeck granules. Immunity, 2000, 12(10: 71-81
5. Engering A, van Vliet SJ, Hebeda K, et al. Dynamic populations of dendritic cell-specific ICAM-3 grabbing nonintegrin-positive immature dendritic cells and liver/lymph node-specific ICAM-3 grabbing nonintegrin-positive endothelial cells in the outer zones of the paracortex of human lymph nodes. Am J Pathol, 2004, 164(5): 1587-1595
6. Albert ML. Death-defying immunity: do apoptotic cells influence antigen processing and presentation? Nat Rev Immunol, 2004, 493): 223-231.
7. Santoro A, Majorana A, Roversi L, et al. Recruitment of dendritic cells in oral lichen planus. J Pathol, 2005, 205(4), 426-434.
8. Kadowaki N, Antonenko S, Lau JY, et al. Natural interferon alpha/beta-producing cells link innate and adaptive immunity. J Exp Med, 2000, 192(2): 219-226.
9. Kirou KA, Vakkalanka RK, Butler MJ, et al. Induction of Fas ligand-mediated apoptosis by interferon-alpha. Clin Immunol, 2000, 95(3): 218-226
10. Christofidou-Solomidou M, Albelda SM, et al. Experimental production and modulation of human cytotoxic dermatitis in human-murine chimeras. Am J Pathol, 1997, 150(2): 631-639.
11. Sugerman PB, Savage NW, Xu LJ, et al. Heat shock protein expression in oral lichen planus. J Oral Pathol Med, 1995, 24(1): 1-8.
12. Younqnak-Piboonratanakit P, Tsushima F, Otsuki n, et al. The expression of B7-H1 on keratinocytes in chronic inflammatory mucocutaneous disease and its regulatory role. Immunol Lett, 2004, 94(3): 215-222.
13. Walsh LJ. Mast cells and oral inflammation. Crit Rev Oral Biol Med, 2003, 14(3):188-198.
14. Zhou XJ, Sugerman PB, Savage NW, et al. Intra-epithelial CD8+ T cells and basement membrane disruption in oral lichen planus. J Oral Pathol Med, 2002, 31(1): 23-27.
15.樊娟丽,白莉.扁平苔藓免疫学研究进展.中国麻风皮肤病杂志, 2005, 21(12):967-969.
16. Khan A, Farah CS, Savage NW, et al. Th1 cytokines in oral lichen planus. J Oral Pathol Med, 2003, 32(2): 77-83.
17. Suqerman PB, Savage NW, Zhou X, et al. Oral lichen planus, Clin Dermatol, 2000, 18(5): 533-539.
18. Simark-Mattsson C, Berqenholtz G, Jontell M, et al. Distribution of interleukin-2, -4, -10, tumour necrosis factor-alpha and transforming growth factor-beta mRNAs in oral lichen planus. Arch Oral Biol, 1999, 44(6): 499-507.
19. Sugerman PB, Savage NW, Seymour GJ, et al. Is there a role for tumour necrosis factor alpha (TNF-alpha) in oral lichen planus? J Oral Pathol Med, 1996, 25(5): 219-224.
20. Sugerman PB, Satterwhite K, Bigby M. Autocytotoxic T-cell clones in lichen planus. Br J Dermatol, 2000, 142(3): 449-456
21. Rich AM, Reade PC. A quantitative assessment of Langerhans cells in oral mucosal lichen planus and leukoplakia. Br J Dermatol, 1989, 120(2): 223-228.
22. Farthing PM, Matear P, Cruchley AT. The activation of Langerhans cells in oral lichen planus. J Oral Pathol Med, 1990, 19(2): 81-85.
23. Albanesi C, Cavani A, Girolomoni G. Interferon-gamma-stimulated human keratinocytes express the genes necessary for the production of peptide-loaded MHC classⅡmolecules. J Invest Dermatol, 1998, 110(2): 138-142.
24. Zhao ZZ, Savage NW, Sugermann PB, et al. Mast cell/T cell interactions in oral lichen planus. J Oral Pathol Med. 2002, 31(4): 189-195.
25. Sistig S, Vucicevic-Boras V, Lukac J, et al. Salivary IgA and IgG subclasses in oral mucosal diseases. Oral Dis, 2002, 8(6): 282-286.
26. Lukac J, Brozovic S, Vucicevic-Boras V, et al. Serum autoantibodies to desmogleins 1 and 3 in patients with oral lichen planus. Croat Med J, 2006, 47(1): 53-58.
27.张学军.皮肤性病学.第5版.北京:人民卫生出版社, 13-15.
28. Simark-Mattsson C, Jontell M, Bergenholtz G, et al. Distribution of interferon-gamma mRNA-positive cells in oral lichen planus lesions. J Oral Pathol Med, 1998, 27(10): 483-488.
29. Simark-Mattsson C, Berqenholtz G, Jontell M, et al. Distribution of interleukin-2, -4, -10, tumour necrosis factor-alpha and transforming growth factor-beta mRNA in oral lichen planus. Arch Oral Biol, 1999, 44(6): 499-507.]
30. Sigidin YA, Loukina GV, Skurkovich B, et al. Randomized, double-blind trial of anti-interferon-gamma antibodies in rheumatoid arthritis. Scand J Rheumatol, 2001, 30(4): 203-207.
31. Leung BP, McInnes IB, Esfandiari E, et al. Combined effects of IL-12 and IL-18 on the induction of collagen-induced arthritis. J Immunol, 2000, 164(12): 6495-6502.
32. Costa GL, Sandora MR, Nakajima A, et al. Adoptive immunotherapy of experimental autoimmune encephalomyelitis via T cell delivery of the IL-12 p40 subunit. J Immunol, 2001, 167(4): 2379-2387.
33. Spandau U, Toksoy A, Goebeler M, et al. MIG is a dominant lymphocyte-attractant chemokine in lichen planus lesions. J Invest Dermatol, 1998, 111(6): 1003-1009.
34. Toruniowa B, Krasowska D, Koziol M, et al. Serum levels of IL-6 in mycosis fungoides, psoriasis and lichen planus. Ann N Y Acad Sci, 1995, 762: 432-434.
35. Toruniowa B, Krasowska D, Koziol M, et al. Serum levels of IL-6 in mycosis fungoides, psoriasis and lichen planus. Ann N Y Acad Sci, 1995, 762: 432-434.
36. Yamamoto T, Yoneda K, Ueta E, et al. Serum cytokines, interleukin-2 receptor, and soluble intercellular adhesion molecule-1 in oral disorders. Oral Surg Oral Med Oral Pathol, 1994, 78(6): 727-735.
37. Sun A, Chia JS, Chang YF, et al. Serum interleukin-6 level is a useful marker inevaluating therapeutic effects of levamisole and Chinese medicinal herbs on patients with oral lichen planus. J Oral Pathol Med, 2002, 31(4): 196-203.
38. Chen F, Castranova V, Shi X. New insights into the role of nuclear factor-kappa B in cell growth regulation. Am J Pathol, 2001, 159(2): 387-397
39. Bours V, Bonizzi G, Bentires-Alj M, et al. NF-kappaB activation in response to toxical and therapeutical agents: role in inflammation and cancer treatment. Toxicology, 2000, 153(1-3): 27-38.
40. Li Q, Verma IM. NF-kappaB regulation in the immune system. Nat Rev Immunol, 2002, 2(10): 725-734.
41. Wan YY, DeGregori J. The survival of antigen-stimulated T cells requires NF kappaB-mediatd inhibition of p73 expression. Immunity, 2003, 18(3): 331-342.
42. Khan A, Farah CS, Savage NW, et al. Th1 cytokines in oral lichen planus. J Oral Pathol Med, 2003, 32(2): 77-83.
43. Sklavounous A, Chrysomali E, Scorilas A, et al. TNF-alpha expression and apoptosis-regulating proteins in oral lichen planus: a comparative immunohistochemical evaluation. J Oral Pathol. Med, 2000, 29(8): 370-375.
44. Sun A, Chia JS, Chang YF, et al. Serum interleukin-6 level is a useful marker in evaluating therapeutic effects of levamisole and Chinese medicinal herbs on patients with oral lichen planus. J Oral Pathol Med, 2002, 31(4): 196-203
45. Santoro A, Majorana A, Bardellini E, et al. NF-kappaB expression in oral and cutaneous lichen planus. J Pathol, 2003, 201(3): 466-472.
46. Pezelj-Ribaric S, Prso IB, Abram M, et al. Salivary levels of tumor necrosis factor-alpha in oral lichen planus. Med inflamm, 2004, 1392): 131-133.