期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 208, 期 5, 页码 1027-1040出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20102149
关键词
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资金
- National Institutes of Health [AI36529, DK45735]
- Deutsche Forschungsgemeinschaft [HU 1714/1-1]
- James Hudson Brown-Alexander B. Coxe Fellowship
- American Cancer Society
- Grants-in-Aid for Scientific Research [21390303] Funding Source: KAKEN
The role of direct IL-10 signaling in different T cell subsets is not well understood. To address this, we generated transgenic mice expressing a dominant-negative IL-10 receptor specifically in T cells (CD4dnIL-10R alpha). We found that Foxp3-depleted CD45RB(lo) (regulatory T cell [T-reg cell]-depleted CD45RB(lo)) but not CD45RB(hi) CD4(+) T cells are controlled directly by IL-10 upon transfer into Rag1 knockout (KO) mice. Furthermore, the colitis induced by transfer of T-reg cell-depleted CD45RB(lo) CD4(+) T cells into Rag1 KO mice was characterized by reduced Th1 and increased Th17 cytokine messenger RNA levels in the colon as compared with the colitis induced by transfer of CD45RB(hi) T cells. In contrast to the CD45RB(hi) transfer colitis model, in which IL-22 is protective, we found that T cell-derived IL-22 was pathogenic upon transfer of T-reg cell-depleted CD45RB(lo) T cells into Rag1 KO mice. Our results highlight characteristic differences between colitis induced by naive (CD45RB(hi)) and memory/ effector (T-reg cell-depleted CD45RB(lo)) cells and different ways that IL-22 impacts inflammatory bowel disease.
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