期刊
JCI INSIGHT
卷 6, 期 21, 页码 -出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/jci.insight.149656
关键词
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资金
- Korea Health Industry Development Institute (KHIDI) - Ministry of Health & Welfare, Republic of Korea [HI18C0479]
- Center for Cancer Research, National Cancer Institute, NIH
Foxp3(+) Tregs in the small intestine epithelium do not require IL-2 for survival and effector functions, exhibiting an independent mechanism and potent suppressor function.
Foxp3(+) Tregs are potent immunosuppressive CD4(+) T cells that are critical to maintain immune quiescence and prevent autoimmunity. Both the generation and maintenance of Foxp3(+) Tregs depend on the cytokine IL-2. Hence, the expression of the IL-2 receptor alpha-chain (CD25) is not only considered a specific marker, but also a nonredundant requirement for Tregs. Here, we report that Foxp3(+) Tregs in the small intestine (SI) epithelium, a critical barrier tissue, are exempt from such an IL-2 requirement, since they had dramatically downregulated CD25 expression, showed minimal STAT5 phosphorylation ex vivo, and were unable to respond to IL-2 in vitro. Nonetheless, SI epithelial Tregs survived and were present at the same frequency as in other lymphoid organs, and they retained potent suppressor function that was associated with high levels of CTLA-4 expression and the production of copious amounts of IL-10. Moreover, adoptive transfer experiments of Foxp3(+) Tregs revealed that such IL-2-independent survival and effector functions were imposed by the SI epithelial tissue, suggesting that tissue adaptation is a mechanism that tailors the effector function and survival requirements of Foxp3(+) Tregs specific to the tissue environment.
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