Id2 represses E2A-mediated activation of IL-10 expression in T cells

Frederick Masson, Margherita Ghisi, Joanna R Groom, Axel Kallies, Cyril Seillet, Ricky W Johnstone, Stephen L Nutt, Gabrielle T Belz

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17 Citations (Scopus)

Abstract

Interleukin-10 (IL-10) is a key immunoregulatory cytokine that functions to prevent inflammatory and autoimmune diseases. Despite the critical role for IL-10 produced by effector CD8+ T cells during pathogen infection and autoimmunity, the mechanisms regulating its production are poorly understood.Weshowthat loss of the inhibitor ofDNA binding 2 (Id2) in T cells resulted in aberrant IL-10 expression in vitro and in vivo during influenza virus infection and in a model of acute graft-versus-host disease (GVHD). Furthermore, IL-10 overproduction substantially reduced the immunopathology associated with GVHD. We demonstrate that Id2 acts to repress the E2A-mediated transactivation of the Il10 locus. Collectively, our findings uncover a key regulatory role of Id2 during effector T cell differentiation necessary to limit IL-10 production by activated T cells and minimize their suppressive activity during the effector phase of disease control.

Original languageEnglish
Pages (from-to)3420-3428
Number of pages9
JournalBlood
Volume123
Issue number22
DOIs
Publication statusPublished - 29 May 2014
Externally publishedYes

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