Increased expression of TIPE2 mRNA in PBMCs of patients with ankylosing spondylitis is negatively associated with the disease severity

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• 作者：Peiqing Zhao^a ; ^b ; ¹ ; Lianqing Wang^a ; ¹ ; Xinxin Xiang^a ; Xiaowei Zhang^a ; Qiaoli Zhai^a ; Xifa Wu^c ; Tao Li^c ; ^{zbszxyyky@163.com}
• 关键词：AS ; ankylosing spondylitis ; TLR ; Toll-like receptor ; TCR ; T cell receptor ; TIPE2 ; tumor necrosis factor α induced protein-8 like-2 ; TIPE1 ; tumor necrosis factor α induced protein-8 like-1 ; PBMCs ; peripheral blood mononuclear cells ; DED ; death effector domain ; BASDAI ; bath ankylosing spondylitis disease activity index ; SLE ; systemic lupus erythematosus ; SpA ; spondyloarthropathies
• 刊名：Human Immunology
• 出版年：2017
• 出版时间：February 2017
• 年：2017
• 卷：78
• 期：2
• 页码：232-237
• 全文大小：923 K
• 卷排序：78

文摘

Ankylosing spondylitis (AS) is an autoimmune disease and characterized by chronic inflammatory arthritis. Tumor necrosis factor α induced protein-8 like-2 (TIPE2) is responsible for maintaining immune homeostasis by inhibiting the secretion of inflammatory cytokines in the condition of inflammation. However, whether TIPE2 participates in the development of AS remains unknown. In this study, we measured the mRNA expression of TIPE2 and TIPE1 in peripheral blood mononuclear cells (PBMCs) from 45 AS patients and 40 healthy controls by qRT-PCR. The results showed TIPE2 expression was significantly increased in AS patients compared with controls (P=0.0066), while there was no significant difference for TIPE1 between two groups (P = 0.2302). Moreover, the expression of TIPE2 mRNA in AS patients were decreased after treatment with TNF-α blocker (P < 0.001). In addition, we found that TNF-α or plasma from AS patients induced TIPE2 expression in THP-1 cells in vitro. More importantly, the TIPE2 mRNA expression levels were negatively correlated with TNF-α, hsCRP and bath ankylosing spondylitis disease activity index (BASDAI) (r = −0.3574, P = 0.0159; r = −0.3174, P = 0.0336; r = −0.6000, P < 0.0001; respectively) in the AS patients. These results indicated that TIPE2 contributes to the pathogenesis of AS.