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

abstract

  • Reports describing the effect of interferon-gamma (IFNgamma) on interleukin-1beta (IL-1beta) production are conflicting. We resolve this controversy by showing that IFNgamma potentiates IL-1beta release from human cells, but transiently inhibits the production of IL-1beta from mouse cells. Release from this inhibition is dependent on suppressor of cytokine signalling 1. IL-1beta and Th17 cells are pathogenic in mouse models for autoimmune disease, which use Mycobacterium tuberculosis (MTB), in which IFNgamma and IFNbeta are anti-inflammatory. We observed that these cytokines suppress IL-1beta production in response to MTB, resulting in a reduced number of IL-17-producing cells. In human cells, IFNgamma increased IL-1beta production, and this might explain why IFNgamma is detrimental for multiple sclerosis. In mice, IFNgamma decreased IL-1beta and subsequently IL-17, indicating that the adaptive immune response can provide a systemic, but transient, signal to limit inflammation.

authors

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

publication date

  • August 2010