(Journal Article): Foxp3 programs the development and function of CD4+CD25+ regulatory T cells.
 
Fontenot JD, Gavin MA, Rudensky AY (Howard Hughes Medical Institute, Department of Immunology, University of Washington, Box 357370, Seattle, WA 98195, USA.)
 
IN: Nat Immunol 2003; 4(4):330-336
Impact Factor(s) of Nat Immunol: 27.011 (2005), 27.586 (2004), 28.18 (2003), 27.868 (2002), 17.431 (2001)

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ABSTRACT: 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+ regulatory T 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 Foxp3-deficient mice. Furthermore, ectopic expression of Foxp3 confers suppressor function on peripheral CD4+CD25- T cells. Thus, Foxp3 is a critical regulator of CD4+CD25+ regulatory T cell development and function.

TYPE OF PUBLICATION: Original article

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