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[炎症性肠病的免疫发病机制]

[Immunopathogenesis of inflammatory bowel diseases].

作者信息

Neurath M F, Schürmann G

机构信息

I. Medizinische Klinik (Direktor: Prof. Dr. P. R. Galle) der Johannes Gutenberg-Universität Mainz.

出版信息

Chirurg. 2000 Jan;71(1):30-40. doi: 10.1007/s001040050005.

Abstract

Inflammatory bowel diseases (IBD: Crohn's disease, ulcerative colitis) are chronic inflammatory and frequently relapsing diseases of the gut that ultimately lead to destruction of the intestinal tissue. Recent evidence suggests that a pathologic activation of the mucosal immune system in response to antigens is a key factor in the pathogenesis of IBD. Furthermore, changes in cell migration and cytokine production appear to contribute to the perpetuation of IBD and the postoperative recurrence of Crohn's disease. Based on recent advances in our understanding of the pathogenesis of IBD, several new therapeutic strategies are currently being tested in clinical practice, including recombinant anti-inflammatory cytokines (IFN-alpha, IL-10, IL-11) and inhibitors of cell adhesion molecules (ICAM), proinflammatory cytokines (TNF, IL-12) and their receptors (TNF, IL-6R).

摘要

炎症性肠病(IBD:克罗恩病、溃疡性结肠炎)是肠道的慢性炎症性且常复发的疾病,最终会导致肠组织破坏。最近的证据表明,黏膜免疫系统对抗原的病理性激活是IBD发病机制中的关键因素。此外,细胞迁移和细胞因子产生的变化似乎有助于IBD的持续存在以及克罗恩病的术后复发。基于我们对IBD发病机制理解的最新进展,目前有几种新的治疗策略正在临床实践中进行测试,包括重组抗炎细胞因子(IFN-α、IL-10、IL-11)以及细胞黏附分子(ICAM)、促炎细胞因子(TNF、IL-12)及其受体(TNF、IL-6R)的抑制剂。

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