Journal article
Regulation of interleukin-1β by interferon-γ is species specific, limited by suppressor of cytokine signalling 1 and influences interleukin-17 production
SL Masters, LA Mielke, AL Cornish, CE Sutton, J O'Donnell, LH Cengia, AW Roberts, IP Wicks, KHG Mills, BA Croker
EMBO Reports | WILEY | Published : 2010
Abstract
Reports describing the effect of interferon-γ (IFNγ) on interleukin-1β (IL-1β) production are conflicting. We resolve this controversy by showing that IFNγ potentiates IL-1β release from human cells, but transiently inhibits the production of IL-1β from mouse cells. Release from this inhibition is dependent on suppressor of cytokine signalling 1. IL-1β and Th17 cells are pathogenic in mouse models for autoimmune disease, which use Mycobacterium tuberculosis (MTB), in which IFNγ and IFNβ are anti-inflammatory. We observed that these cytokines suppress IL-1β production in response to MTB, resulting in a reduced number of IL-17-producing cells. In human cells, IFNγ increased IL-1β production, a..
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Awarded by National Health and Medical Research Council
Funding Acknowledgements
This study was supported by a National Health and Medical Research Council Program Grant (461219); National Health and Medical Research Council Independent Research Institutes Support Scheme Grant (361646); Victorian State Government Operational Infrastructure Support Grant and National Institutes of Health Grant CA022556; National Health and Medical Research Council Overseas Biomedical Fellowship (SLM, 516783); National Health and Medical Research Council Career Development Award (to B. A. C., 575531); National Health and Medical Research Council Peter Doherty Fellowship (to A. L. C.); National Health and Medical Research Council Practitioner Fellowship and Reid Charitable Trusts (to I. P. W.); National Health and Medical Research Council Practitioner Fellowship (to A. W. R., 637309) and a Victorian Cancer Agency Fellowship (to A. W. R.). The part of the study conducted at Trinity College, Dublin, was supported by Science Foundation Ireland.