Mucosal Immunity and Inflammation II. The yin and yang of T cells in intestinal inflammation: pathogenic and protective roles in a mouse colitis model
Mucosal Immunity and Inflammation II. The yin and yang of T cells in intestinal inflammation: pathogenic and protective roles in a mouse colitis model
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DOI：
10.1152/ajpgi.1999.276.6.g1317
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发表时间：
1999-06-01
影响因子：
4.5
通讯作者：
Kronenberg, M
中科院分区：
文献类型：
--
作者：
De Winter, H;Cheroutre, H;Kronenberg, M
炎症性肠病（IBD）是一种病因不明的多因素免疫疾病。几种类似IBD的小鼠粘膜炎症模型的出现，为正常和病理粘膜免疫功能的调控机制提供了见解。在一种广泛使用的过继转移模型中，向免疫缺陷小鼠注射CD4(+) T淋巴细胞亚群，CD4(+)CD45RB（高）细胞，导致肠道炎症。发病机制部分是由于促炎细胞因子的分泌。结肠炎的诱导可以通过另一种CD4（+）亚群，CD4(+)CD45RB（低）T细胞的共转移来预防。该群体的行为类似于CD4(+)CD45RB（高）群体在获得激活标记和归巢到宿主肠道方面的行为。然而，当它们被激活时，它们的淋巴因子谱是不同的，CD4(+)CD45RB（低）T细胞分泌和/或诱导的抗炎细胞因子可以预防结肠炎。在这篇主题文章中，对过继转移模型进行了描述，讨论了促进和预防结肠炎发病的因素，并对该模型的一些有争议的方面进行了讨论。
Inflammatory bowel disease (IBD) is a multifactorial immune disorder of uncertain etiology. The advent of several mouse models of mucosal inflammation that resemble IBD has provided insight into the mechanisms governing both normal and pathological mucosal immune function. In a widely used adoptive transfer model, the injection into immunodeficient mice of a subset of CD4(+) T lymphocytes, the CD4(+)CD45RB(high) cells, leads to inflammation of the intestine. Pathogenesis is due in part to the secretion of proinflammatory cytokines. The induction of colitis can be prevented by cotransfer of another CD4(+) subpopulation, the CD4(+)CD45RB(low) T cells. This population behaves analogously to the CD4(+)CD45RB(high) population in terms of the acquisition of activation markers and homing to the host intestine. However, their lymphokine profile when activated is different, and anti-inflammatory cytokines secreted and/or induced by CD4(+)CD45RB(low) T cells prevent colitis. In this themes article, a description of the adoptive transfer model is given, the factors that promote and prevent colitis pathogenesis are discussed, and some controversial aspects of the model are addressed.