期刊
JOURNAL OF IMMUNOLOGY
卷 198, 期 3, 页码 986-992出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.1038/ni904
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类别
资金
- National Institutes of Health
- Cancer Research Institute
- Howard Hughes Medical Institute
CD4(+)CD25(+) regulatory T cells are essential for the active suppression of autoimmunity. Here we report that the forkhead transcription factor Foxp3 is specifically expressed in CD4+CD25+ regulatoryT cells and is required for their development.The lethal autoimmune syndrome observed in Foxp3-mutant scurfy mice and Foxp3-null mice results from a CD4+CD25+ regulatory T cell deficiency and not from a cell-intrinsic defect of (CD4+CD25)-T cells. CD4+CD25+ regulatory T cells rescue disease development and preferentially expand when transferred into neonatal Foxp3deficient mice. Furthermore, ectopic expression of Foxp3 confers suppressor function on peripheral (CD4+CD25)-T cells. Thus, Foxp3 is a critical regulator of CD4+CD25+ regulatoryT cell development and function.
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