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TSLP 在炎症性肠病中的作用研究进展。

Insight into the role of TSLP in inflammatory bowel diseases.

机构信息

Yonsei University College of Medicine, Seoul, Korea.

Inserm U954 and Department of Gastroenterology, Nancy University Hospital, Université de Lorraine, France.

出版信息

Autoimmun Rev. 2017 Jan;16(1):55-63. doi: 10.1016/j.autrev.2016.09.014. Epub 2016 Oct 1.

Abstract

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.

摘要

促炎细胞因子被认为调节各种炎症性肠病(IBD)的发病机制。胸腺基质淋巴细胞生成素(TSLP)在哮喘、特应性皮炎(AD)和嗜酸性食管炎(EoE)等各种过敏性疾病中进行了研究,而在 IBD 中则较少被认为涉及。然而,据报道,包括 TSLP 在内的各种细胞因子诱导的黏膜树突状细胞(DC)导致 T 细胞向 Th2 反应、调节性 T 细胞(Treg)分化和 B 细胞分泌 IgA 的极化。在这篇综述中,我们讨论了这样一个概念,即 TSLP 的减少有可能加速 Th1 反应占主导的疾病(如克罗恩病(CD))的发展,而 TSLP 的增加则有可能导致 Th2 细胞占主导的疾病(如溃疡性结肠炎(UC))的发展。为了研究 TSLP 作为区分 UC 和 CD 的潜在决定因素的作用,我们使用来自 NetPath、GeneMania 和 String 数据库等在线开放资源的其他受 TSLP 调节的基因的数据,分析了其对 UC 和 CD 发病机制的影响。我们的研究结果表明,TSLP 是 IBD 发病机制中的关键介质,需要进一步研究以评估其作用。

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