期刊
JOURNAL OF IMMUNOLOGY
卷 179, 期 3, 页码 1427-1430出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.179.3.1427
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- NCI NIH HHS [CA91837] Funding Source: Medline
- NIAID NIH HHS [AI070535] Funding Source: Medline
Naive CD4 T cells can develop into regulatory T cells by acquiring the transcription factor Foxp3. Combined signals from the TCR, CD28, IL-2R, and TGF-beta R promote Foxp3 expression in activated naive CD25(-) CD4 T cells. Here we show that OX40 (CD134) signaling inhibits TGF-beta-driven Foxp3 mRNA and suppresses the conversion of naive Ag-specific transgenic CD4 Tcells into CD25(+)Foxp3(+) T cells. These data identify OX40 as a negative regulator of Foxp3 and suggest that OX40 can concomitantly promote effector T cell generation while antagonizing the differentiation of adaptive Foxp3(+) regulatory T cells.
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