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The function of Foxp3 independent of suppressive activity
Author(s) -
Han Shuhua,
Guo Linjie
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.661.20
Subject(s) - foxp3 , il 2 receptor , immune system , transgene , immunology , phenotype , effector , inflammation , regulatory t cell , biology , microbiology and biotechnology , genetically modified mouse , t cell , genetics , gene
The forkhead family transicrption factor Foxp3 is critically important for the development and function of regulatory T cells (Tregs). Lack of Foxp3 leads to the development of fatal autoimmune lymphoproliferative diseases. Previously studies have shown that ectopic Foxp3 expression can phenotypically convert effector T cells to regulatory T cells. However, we have recently generated Foxp3 transgenic mice under the control of lck distal promoter. Our data showed that enforced Foxp3 expression rendered CD4+CD25– T cells hyporesponsive but conferred neither Treg phenotype nor suppressive function. When Foxp3 transgenic mice were crossed to scurfy mice, the scurfy phenotype was partially rescued but the lymphoproliferative disease was still apparent. Thus, Foxp3 expression, presumably depending on its expression levels, can result in distinct effects on the functions of CD4+ T cells. In addition, we found that Foxp3 transgenic mice exhibit reduced susceptibility to collagen‐induced arthritis (CIA). Therefore, Foxp3 may play important roles in regulating immune responses and inflammation independent of suppressive function.