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The NF-κB transcription factor RelA is required for the tolerogenic function of Foxp3(+) regulatory T cells.

Messina N, Fulford T, O'Reilly L, Loh WX, Motyer JM, Ellis D, McLean C, Naeem H, Lin A, Gugasyan R, Slattery RM, Grumont RJ, Gerondakis S

  • Journal Journal of autoimmunity

  • Published 07 Apr 2016

  • Volume 70

  • Pagination 52-62

  • DOI 10.1016/j.jaut.2016.03.017


The properties of CD4(+) regulatory T cell (Treg) subsets are dictated by distinct patterns of gene expression determined by FOXP3 and different combinations of various transcription factors. Here we show the NF-κB transcription factor RelA is constitutively active in naïve and effector Tregs. The conditional inactivation of Rela in murine FOXP3(+) cells induces a rapid onset, multi-focal autoimmune disease that depends on RelA being expressed in conventional T cells. In addition to promoting Treg lineage stability, RelA determines the size of the effector Treg population, a function influenced by the presence or absence of RelA in conventional T cells. These findings showing that RelA controls Treg stability and promotes the competitive fitness of effector Tregs highlight the importance of RelA activity in peripheral Treg induced tolerance.