期刊
BLOOD
卷 123, 期 22, 页码 3420-3428出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2014-03-561456
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资金
- National Health and Medical Research Council of Australia (NHMRC) [APP1042582]
- Australian Research Council
- Leukemia Foundation of Australia
- Victorian Cancer Agency
- Victorian State Government Operational Infrastructure Support
- Australian Government NHMRC IRIIS
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 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.
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