期刊
IMMUNITY
卷 35, 期 1, 页码 109-122出版社
CELL PRESS
DOI: 10.1016/j.immuni.2011.03.029
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资金
- National Institutes of Health [R01 AI073731, R01 AI085090, N01 50032, R01 AI065617, R01 AI078713]
- D.B. and Marjorie Reinhart Foundation
- Montgomery Family Foundation
- Advancing a Healthier Wisconsin-Research for a Healthier Tomorrow Initiative
- Crohn's and Colitis Foundation of America
- Children's Hospital of Wisconsin
Although both natural and induced regulatory T (nTreg and iTreg) cells can enforce tolerance, the mechanisms underlying their synergistic actions have not been established. We examined the functions of nTreg and iTreg cells by adoptive transfer immunotherapy of newborn Foxp3-deficient mice. As monotherapy, only nTreg cells prevented disease lethality, but did not suppress chronic inflammation and autoimmunity. Provision of Foxp3-sufficient conventional T cells with nTreg cells reconstituted the iTreg pool and established tolerance. In turn, acute depletion of iTreg cells in rescued mice resulted in weight loss and inflammation. Whereas the transcriptional signatures of nTreg and in vivo-derived iTreg cells were closely matched, there was minimal overlap in their T cell receptor (TCR) repertoires. Thus, iTreg cells are an essential nonredundant regulatory subset that supplements nTreg cells, in part by expanding TCR diversity within regulatory responses.
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