Control of experimental inflammatory bowel disease by regulatory T cells
Control of experimental inflammatory bowel disease by regulatory T cells
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DOI：
10.1164/ajrccm.162.supplement_3.15tac9
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发表时间：
2000-10-01
影响因子：
24.7
通讯作者：
Powrie, F
中科院分区：
文献类型：
--
作者：
Asseman, C;Fowler, S;Powrie, F
在CD45Rb(高)CD4(+)T细胞转移后，由肠道细菌驱动的辅助T细胞1型介导的结肠炎在严重的联合免疫缺陷小鼠中发生。疾病的发生可以通过CD45RB(低)亚群的相互转移来预防。对CD45RB(Low)CD4(+)细胞转移免疫抑制机制的分析揭示了IL-10和转化生长因子-β的重要作用。这些数据表明，在正常小鼠中存在功能专门化的调节性T(Treg)细胞群，这些细胞可以防止对共生细菌的致病反应的发展。对Treg细胞在免疫反应控制中的作用进行了讨论。
A helper T cell type 1-mediated colitis driven by enteric bacteria develops in severe combined immunodeficient mice after transfer of CD45RB(high)CD4(+) T cells. Development of disease can be prevented by cotransfer of the reciprocal CD45RB(low) subset. Analysis of the mechanism of immune suppression transferred by CD45RB(low)CD4(+) cells revealed essential roles for both IL-10 and TGF-beta. These data indicate that a functionally specialized population of regulatory T (Treg) cells exists in normal mice and that these can prevent the development of pathogenic responses toward commensal bacteria. The role of Treg cells in the control of the immune response is discussed.