Insight into the role of TSLP in inflammatory bowel diseases

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• 作者：Jae Hyon Park^a ; ¹ ; Dong Yeon Jeong^a ; ¹ ; Laurent Peyrin-Biroulet^b ; Michael Eisenhut^c ; Jae Il Shin^d ; ^{shinji@yuhs.ac}
• 关键词：Thymic stromal lymphopoietin ; Immuno-pathogenesis ; Inflammatory bowel disease ; Gene-to-gene network ; Protein-to-protein network
• 刊名：Autoimmunity Reviews
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：16
• 期：1
• 页码：55-63
• 全文大小：698 K
• 卷排序：16

文摘

Proinflammatory cytokines are thought to modulate pathogeneses of various inflammatory bowel diseases (IBDs). Thymic stromal lymphopoietin (TSLP), which has been studied in various allergic diseases such as asthma, atopic dermatitis (AD) and eosinophilic esophagitis (EoE), has been less considered to be involved in IBDs. However, mucosal dendritic cells (DCs) induced by various cytokines including TSLP were reported to cause polarization of T cell toward Th2 response, the differentiation of regulatory T-cell (Treg), and secretion of IgA by B cells. In this review, we discuss the concept that decreased TSLP has the potential to accelerate the development of Th1 response dominant diseases such as the Crohn's disease (CD) while increased TSLP has the potential to lead to a development of Th2 cell dominant diseases such the ulcerative colitis (UC). To examine TSLP's role as a potential determining factor for differentiating UC and CD, we analyzed the effects of other genes regulated by TSLP in regards to the UC and CD pathogeneses using data from online open access resources such as NetPath, GeneMania, and the String database. Our findings indicate that TSLP is a key mediator in the pathogenesis of IBDs and that further studies are needed to evaluate its role.