학술논문
The NF-κB transcription factor RelA is required for the tolerogenic function of Foxp3+ regulatory T cells.
Document Type
Article
Author
Source
Subject
*T cells
*GENE expression
*TRANSCRIPTION factors
*AUTOIMMUNE diseases
*SCURFIN (Protein)
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Language
ISSN
0896-8411
Abstract
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. [ABSTRACT FROM AUTHOR]