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Blood. 2014 May 29;123(22):3420-8. doi: 10.1182/blood-2014-03-561456. Epub 2014 Apr 10.

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

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  • 1Division of Molecular Immunology Division, Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia; Department of Medical Biology, University of Melbourne, Melbourne, Australia;
  • 2Peter MacCallum Cancer Centre, Melbourne, Australia; and.
  • 3Peter MacCallum Cancer Centre, Melbourne, Australia; and Sir Peter MacCallum Department of Oncology, University of Melbourne, Melbourne, Australia.

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. We show that loss of the inhibitor of DNA 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 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.

© 2014 by The American Society of Hematology.

[PubMed - indexed for MEDLINE]
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