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.