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In humans, there are 4 distinct interleukin-36 genes. They are, three receptor agonists: IL36A, IL36B, and IL36G, and one receptor antagonist IL36RA that bind the IL-36 receptor (IL1RL2/IL-1Rrp2/IL-36 receptor) with varying affinities. The agonists are known to activate NF-κB and mitogen-activated protein kinases to induce various proinflammatory mediators. [1] It has also been found to activate T cell proliferation and release of IL-2.[2] Due to their predominant expression in epithelial tissues, IL-36 cytokines are believed to play a significant role in the pathogenesis of skin diseases, especially that of psoriasis.[3]


  1. ^ Towne JE, Renshaw BR, Douangpanya J, Lipsky BP, Shen M, Gabel CA, Sims JE (December 2011). "Interleukin-36 (IL-36) ligands require processing for full agonist (IL-36α, IL-36β, and IL-36γ) or antagonist (IL-36Ra) activity". J. Biol. Chem. 286 (49): 42594–602. doi:10.1074/jbc.M111.267922. PMC 3234937Freely accessible. PMID 21965679. 
  2. ^ Vigne S, Palmer G, Martin P, Lamacchia C, Strebel D, Rodriguez E, Olleros ML, Vesin D, Garcia I, Ronchi F, Sallusto F, Sims JE, Gabay C (October 2012). "IL-36 signaling amplifies Th1 responses by enhancing proliferation and Th1 polarization of naive CD4+ T cells". Blood. 120 (17): 3478–87. doi:10.1182/blood-2012-06-439026. PMID 22968459. 
  3. ^ Gresnigt MS, van de Veerdonk FL (December 2013). "Biology of IL-36 cytokines and their role in disease". Seminars in Immunology. 25 (6): 458–65. doi:10.1016/j.smim.2013.11.003. PMID 24355486.