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

Autor: Messina N; Biomedicine Discovery Institute, Monash University, Clayton, Victoria 3800, Australia; Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria 3800, Australia., Fulford T; Biomedicine Discovery Institute, Monash University, Clayton, Victoria 3800, Australia; Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria 3800, Australia., O'Reilly L; Walter and Eliza Hall Institute of Medical Research, 1G, Parkville, Victoria 3052, Australia; Department of Medical Biology, The University of Melbourne, Parkville, Victoria 3050, Australia., Loh WX; Department of Immunology, Monash University Central Clinical School, Prahran, Victoria 3004, Australia., Motyer JM; Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria 3800, Australia., Ellis D; Biomedicine Discovery Institute, Monash University, Clayton, Victoria 3800, Australia; Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria 3800, Australia., McLean C; Department of Anatomical Pathology, The Alfred Hospital, Prahran, Victoria 3004, Australia., Naeem H; Monash Bioinformatics Platform, Monash University, Clayton, Victoria 3800, Australia., Lin A; Walter and Eliza Hall Institute of Medical Research, 1G, Parkville, Victoria 3052, Australia., Gugasyan R; The Burnet Institute, Prahran, Victoria 3004, Australia., Slattery RM; Department of Immunology, Monash University Central Clinical School, Prahran, Victoria 3004, Australia., Grumont RJ; Biomedicine Discovery Institute, Monash University, Clayton, Victoria 3800, Australia; Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria 3800, Australia., Gerondakis S; Biomedicine Discovery Institute, Monash University, Clayton, Victoria 3800, Australia; Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria 3800, Australia. Electronic address: steven.gerondakis@monash.edu.
Jazyk: angličtina
Zdroj: Journal of autoimmunity [J Autoimmun] 2016 Jun; Vol. 70, pp. 52-62. Date of Electronic Publication: 2016 Apr 07.
DOI: 10.1016/j.jaut.2016.03.017
Abstrakt: 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.
(Copyright © 2016 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
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