期刊
JOURNAL OF IMMUNOLOGY
卷 190, 期 11, 页码 5788-5798出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1203111
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资金
- Ministry of Education, Science, Sports, and Culture of Japan
- Japan Society for the Promotion of Science
- Japan Science and Technology Agency
- Sumitomo Foundation
- Uehara Memorial Foundation
- Novartis Foundation for the Promotion of Science
- Yakult Bio-Science Foundation
- Grants-in-Aid for Scientific Research [24659487, 11J06848, 24390118] Funding Source: KAKEN
Homeostatic proliferation of naive T cells in the spleen and cutaneous lymph nodes supplies memory phenotype T cells. The systemic proliferative responses divide distinctly into fast or slow cell division rates. The fast proliferation is critical for generation of effector memory T cells. Because effector memory T cells are abundant in the lamina propria of the intestinal tissue, gut-specific homeostatic proliferation of naive T cells may be important for generation of intestinal effector memory T cells. However, such organ-specific homeostatic proliferation of naive T cells has not yet been addressed. In this study, we examined the gut-specific homeostatic proliferation by transferring CFSE-labeled naive CD4(+) T cells into sublethally irradiated mice and separately evaluating donor cell division and differentiation in the intestine, mesenteric lymph nodes (MLNs), and other lymphoid organs. We found that the fast-proliferating cell population in the intestine and MLNs had a gut-tropic alpha(4)beta(+)(7) Th17 phenotype and that their production was dependent on the presence of commensal bacteria and OX40 costimulation. Mesenteric lymphadenectomy significantly reduced the Th17 cell population in the host intestine. Furthermore, FTY720 treatment induced the accumulation of alpha(4)beta+7IL-17A(+) fast-dividing cells in MLNs and eliminated donor cells in the intestine, suggesting that MLNs rather than intestinal tissues are essential for generating intestinal Th17 cells. These results reveal that MLNs play a central role in inducing gut-tropic Th17 cells and in maintaining CD4(+) T cell homeostasis in the small intestine.
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