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

Nicole Messina, Thomas Fulford, Lorraine O'Reilly, Wen Xian Loh, Jessica M. Motyer, Darcy Ellis, Catriona McLean, Haroon Naeem, Ann Lin, Raffi Gugasyan, Robyn M. Slattery, Raelene J. Grumont, Steve Gerondakis

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32 Citations (Scopus)


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.
Original languageEnglish
Pages (from-to)52-62
Number of pages11
JournalJournal of Autoimmunity
Publication statusPublished - Jun 2016


  • Regulatory T cells
  • Nuclear factor of kappaB
  • RelA
  • Conditional gene targeting
  • Autoimmune disease

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