The IL-1 family of cytokines comprises 11 members, including IL-1alpha, IL-1beta, IL-18, IL-33, and three IL-36 homologues, namely IL-36alpha, IL-36beta, IL-36gamma (previously termed IL-1F6, IL-1F8, IL-1F9). IL-36 binds to IL-36R (previously termed IL-1Rrp2) leading to the recruitment of IL-1RAcP and intracellular signals similar to those induced by other IL-1 cytokines. Natural inhibitors control the biological activities of IL-1 cytokines. IL-1 receptor antagonist (IL-1Ra) is a cytokine that inhibits IL-1 activities by competitively blocking its interaction with cell surface receptors. IL-36Ra exerts the same type of inhibitory activities for IL-36. Hereditary deficiency of IL-36Ra leads to a severe form generalized pustular psoriasis, indicating that the IL-36/IL-36Ra balance is critical for the control of skin inflammation. Experimental data from animal models and human samples suggest that IL-36 is involved in the pathogenesis of psoriasis.
Recently, my laboratory has shown that IL-36 exerts strong stimulatory effects on dendritic cells, leading to cytokine release and increased expression of MHC class 2 and co-stimulatory molecules. IL-36 stimulates the polarization of of naïve CD4+ T cells into interferon-gamma producing Th1 cells in vitro and in vivo. Taken together these data indicate that IL-36 stimulates both innate and adaptive immune responses that may be critical for host responses to pathogens and inflammatory conditions.
Take home message:
The family of IL-1 cytokines includes several members with different biologic functions
IL-36 is a novel member of the IL-1 family of cytokines, the activity of which is controlled by IL-36Ra
Several evidence suggest that IL-36 is involved skin psoriasis
IL-36 exerts stimulatory activities leading to Th1 responses
Disclosure of Interest None Declared
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