期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 197, 期 1, 页码 111-119出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20021345
关键词
regulatory T cells; helicobacter; immune tolerance; mucosal immunity; IL-10
资金
- Wellcome Trust Funding Source: Medline
CD4(+)CD25(+) regulatory T (T-R) cells can inhibit a variety of autoimmune and inflammatory diseases, but the precise mechanisms by which they suppress immune responses in vivo remain unresolved. Here, we have used Helicobacter hepaticus infection of T cell-reconstituted recombination-activating gene (RAG)(-/-) mice as a model to study the ability of CD4(+)CD25(+) T-R cells to inhibit bacterially triggered intestinal inflammation. H. hepaticus infection elicited both T cell-mediated and T cell-independent intestinal inflammation, both of which were inhibited by adoptively transferred CD4(+)CD25(+) T-R cells. T cell-independent pathology was accompanied by activation of the innate immune system that was also inhibited by CD4(+)CD25(+) T-R cells. Suppression of innate immune pathology was dependent on T cell-derived interleukin 10 and also on the production of transforming growth factor beta. Thus, CD4(+)CD25(+) T-R cells do not only suppress adaptive T cell responses, but are also able to control pathology mediated by innate immune mechanisms.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据