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FoxP3 (red) is expressed on cortical epithelial cells (green) and drives thymocyte proliferation.

On page 1141, the one-trick transcription factor FoxP3 reveals a new function. According to Chang and colleagues, FoxP3 does more than just drive regulatory T (T reg) cell development; it also promotes the proliferation of developing thymocytes.

FoxP3 is required for the development of CD4⁺CD25⁺ T reg cells, which subdue the activation of conventional T cells and thus protect against chronic inflammation and autoimmunity. Mice and humans that lack FoxP3 develop a spontaneous, multi-organ autoimmune disease that has been primarily attributed to the lack of T reg cells. But one fact suggests that this explanation may be too simple. Irradiated mice that are reconstituted with FoxP3-deficient bone marrow do not develop disease, suggesting that FoxP3 also functions in nonhematopoietic cells.

Chang and colleagues now show that FoxP3 is not exclusive to T cells, but is also expressed in thymic epithelial cells. In mice lacking FoxP3, developing thymocytes were unable to proliferate normally, resulting in thymic atrophy. The proliferation defect was caused by a lack of FoxP3 in thymic stromal cells, rather than in T cells, as normal thymocytes also failed to proliferate in a FoxP3-deficient thymic environment.How FoxP3 expression on thymic epithelial cells helps drive thymocyte proliferation is unknown. Also unclear is how the proliferation defect contributes to autoimmune disease, although there is a long-standing but poorly understood link between thymic atrophy and T cell–driven autoimmune disease.

hvanepps{at}rockefeller.edu

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This Article Full Text (PDF, 848K) PPT slides of all figures Alert me when this article is cited Services Email this article Similar articles in this journal Alert me to new content in the JEM Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Van Epps, H. L. Search for Related Content PubMed Articles by Van Epps, H. L. Related Collections Related Article Social Bookmarking                            What's this?