Regulation of interleukin-1β by interferon-γ is species specific, limited by suppressor of cytokine signalling 1 and influences interleukin-17 production

Seth L. Masters, Lisa A. Mielke, Ann L. Cornish, Caroline E. Sutton, Joanne O'Donnell, Louise H. Cengia, Andrew W. Roberts, Ian P. Wicks, Kingston H G Mills, Ben A. Croker

Research output: Contribution to journalArticleResearchpeer-review

48 Citations (Scopus)

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, and this might explain why IFNγ is detrimental for multiple sclerosis. In mice, IFNγ decreased IL-1β and subsequently IL-17, indicating that the adaptive immune response can provide a systemic, but transient, signal to limit inflammation.

Original languageEnglish
Pages (from-to)640-646
Number of pages7
JournalEMBO Reports
Volume11
Issue number8
DOIs
Publication statusPublished - Aug 2010
Externally publishedYes

Keywords

  • IFNg
  • IL-17
  • IL-1b
  • inflammasome
  • SOCS1

Cite this