Foxp3-deficient regulatory T cells do not revert into conventional effector CD4+ T cells but constitute a unique cell subset.

ABSTRACT: Homeostasis in the immune system is maintained by specialized regulatory CD4(+) T cells (T(reg)) expressing transcription factor Foxp3. According to the current paradigm, high-affinity interactions between TCRs and class II MHC-peptide complexes in thymus "instruct" developing thymocytes to up-regulate Foxp3 and become T(reg) cells. However, the loss or down-regulation of Foxp3 does not disrupt the development of T(reg) cells but abrogates their suppressor function. In this study, we show that Foxp3-deficient T(reg) cells in scurfy mice harboring a null mutation of the Foxp3 gene retained cellular features of T(reg) cells including in vitro anergy, impaired production of inflammatory cytokines, and dependence on exogenous IL-2 for proliferation and homeostatic expansion. Foxp3-deficient T(

SUBMITTER: Kuczma M 

PROVIDER: S-EPMC2771373 | biostudies-literature | 2009 Sep

REPOSITORIES: biostudies-literature