| First Author | Masson F | Year | 2014 |
| Journal | Blood | Volume | 123 |
| Issue | 22 | Pages | 3420-8 |
| PubMed ID | 24723679 | Mgi Jnum | J:213132 |
| Mgi Id | MGI:5582959 | Doi | 10.1182/blood-2014-03-561456 |
| Citation | Masson F, et al. (2014) Id2 represses E2A-mediated activation of IL-10 expression in T cells. Blood 123(22):3420-8 |
| abstractText | 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. |
