Id2 represses E2A-mediated activation of IL-10 expression in T cells
Details
Publication Year 2014-04-10,Volume 123,Issue #22,Page 3420-8
Journal Title
Blood
Publication Type
Journal Article
Abstract
Interleukin (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. We show that loss of the Inhibitor of DNA binding (Id) 2 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 vs. host disease (GVHD). Furthermore, IL-10 over-production substantially reduced the immunopathology associated with GVHD. We demonstrate that Id2 acts to repress the E2A-mediated trans-activation 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.
Publisher
AMER SOC HEMATOLOGY
Research Division(s)
Cell Signalling And Cell Death; Molecular Immunology
NHMRC Grants
NHMRC/1042582
Terms of Use/Rights Notice
Copyright © 2014 American Society of Hematology


Creation Date: 2014-04-16 08:43:43
Last Modified: 2015-09-07 12:18:10
An error has occurred. This application may no longer respond until reloaded. Reload 🗙