Journal
EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 37, Issue 7, Pages 1817-1826Publisher
WILEY
DOI: 10.1002/eji.200737101
Keywords
foxp3; IL-2; regulatory T cells
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Funding
- NIAID NIH HHS [AI48779] Funding Source: Medline
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Immunological tolerance to self antigens is a tightly regulated process. Recent work has demonstrated that the forkhead family member Foxp3 is a critical element in the differentiation and function of mouse CD4(+)CD25(+) regulatory T cells (Treg). Recent work has suggested an important role for IL-2 in the development and maintenance of Treg. To directly assess the effect of IL-2 signaling on Treg development and function, we analyzed mice that were genetically deficient in components of the IL-2 receptor (IL-2R). Mice lacking CD25 (IL-2R alpha) displayed a slight decrease in Treg within the thymus, while peripheral numbers are unchanged. In contrast, we found that mice deficient in CD122 (IL-2R beta) had a profound reduction in both thymic and peripheral Treg, coinciding with more rapid development of a fatal lymphoproliferative disease. Expression of a Foxp3 transgene restored Treg and protected against the onset of autoimmunity. Thus, a signal mediated by IL-2R beta is essential for the development and homeostasis of Foxp3(+) Treg in vivo.
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