The IL-1 family is a group of cytokines comprised of 11 members, including the recently renamed IL-36 cytokines, IL-36α, β, and γ (previously known as IL-1F6, IL-1F8, and IL-1F9, respectively). IL-36γ signals through the IL-1 receptor family members IL-1Rrp2 and IL-1RAcP and can activate downstream MAP kinases and transcription factor NF-κB. IL-36γ is synthesized without signal peptide and the secretion pathway is unclear. It has been shown that like other IL-36 cytokines, the N-terminal processing of IL-36γ can significantly increase its biological activity. The possible processing enzymes are currently unknown. IL-36γ plays a significant role in the immune response, as low levels of IL-36 receptor IL-1Rrp can be detected on bone marrow-derived dendritic cells and CD4+ T cells. IL-36γ treatment can upregulate CD80, CD86 and MHC Class II, and proinflammatory cytokine production in dendritic cells. IL-36γ has also been implicated in airway hyperesponsiveness. Intranasal administration of recombinant IL-36γ in mice leads to epithelial cell hypertrophy, cellular infiltration, and mucus production. IL-36γ expression in the lungs of mice can be upregulated by allergic inflammation. In the skin, IL-36γ is primarily expressed by keratinocytes and its expression can be upregulated by inflammatory cytokines, toll-like receptor ligands, and some pathological conditions. IL-36γ is highly induced in psoriasis plaques. ???