炎症性肠病
免疫学
回肠炎
免疫系统
炎症
实验性自身免疫性脑脊髓炎
T细胞
医学
肿瘤坏死因子α
结肠炎
关节炎
克罗恩病
疾病
内科学
作者
Anja A. Kühl,Christoph Loddenkemper,Jürgen Westermann,Jörg Hoffmann
出处
期刊:Pathobiology
[S. Karger AG]
日期:2002-01-01
卷期号:70 (3): 150-155
被引量:24
摘要
gammadelta T cells have previously been shown to play a protective role in various animal models of chronic inflammation (e.g., experimental autoimmune encephalomyelitis, collagen-induced arthritis, and non-obese diabetes). This immunoregulatory potential is exerted by synthesizing various anti-inflammatory cytokines and growth factors (e.g., transforming growth factor-beta). As the normal balance between inflammatory and regulatory cytokines is perturbed in inflammatory bowel disease (IBD) a protective effect of gammadelta T cells seems likely. This notion is supported by our finding of increased mortality of rats with 2,4,6-trinitrobenzene sulfonic acid-induced colitis following gammadelta T cell depletion. In contrast, no effect was observed after depletion of gammadelta T cells in a Crohn's disease animal model with terminal ileitis (TNF(DeltaARE) mice). Therefore, future studies must further define where in the intestinal immune system gammadelta T cells exert their protective function and how this can be used in the treatment of IBD.
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