Journal article
Id2 represses E2A-mediated activation of IL-10 expression in T cells
F Masson, M Ghisi, JR Groom, A Kallies, C Seillet, RW Johnstone, SL Nutt, GT Belz
Blood | Published : 2014
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 lo..
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Awarded by National Health and Medical Research Council of Australia (NHMRC)
Funding Acknowledgements
J.R.G. was supported by a National Health and Medical Research Council of Australia (NHMRC) training fellowship, and G. T. B. and S.N. were supported by Australian Research Council future fellowships. R.W.J. is a principal research fellow of the NHMRC and supported by NHMRC program and project grants, The Leukemia Foundation of Australia, and the Victorian Cancer Agency. This work was supported by a project grant (APP1042582) from the NHMRC and Victorian State Government Operational Infrastructure Support and Australian Government NHMRC IRIIS.