期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 201, 期 7, 页码 1061-1067出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20042276
关键词
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资金
- NIAID NIH HHS [R01 AI061816, R37 AI034206, AI061816, R01 AI034206, AI34206] Funding Source: Medline
Transforming growth factor (TGF)-beta 1 is a major pluripotential cytokine with a pronounced immunosuppressive effect and its deficiency results in lethal autoimmunity in mice. However, mechanisms of its immunosuppressive action are not completely understood. Here, we report that TGF-beta 1 supports the maintenance of Foxp3 expression, regulatory function, and homeostasis in peripheral CD4(+)CD25(+) regulatory T ( T reg) cells, but is not required for their thymic development. We found that in 8-10-d-old TGF-beta 1-deficient mice, peripheral, but not thymic, T reg cells are significantly reduced in numbers. Moreover, our experiments suggest that a defect in TGF-beta-mediated signaling in T reg cells is associated with a decrease in Foxp3 expression and suppressor activity. Thus, our results establish an essential link between TGF-beta 1 signaling in peripheral T reg cells and T reg cell maintenance in vivo.
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