Interleukin 36

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"IL-36" redirects here. For the road formerly known as Illinois Route 36, see Illinois Route 94.

Interleukin 36, or IL-36, is a group of cytokines in the IL-1 family with pro-inflammatory effects. The role of IL-36 in inflammatory diseases is under investigation.[1]

There are four members of the IL-36 family which bind to the IL-36 receptor (IL1RL2/IL-1Rrp2/IL-36 receptor dimer) with varying affinities.[2] IL36A, IL36B, and IL36G are IL-36 receptor agonists. IL36RA is an IL-36 receptor antagonist, inhibiting IL-36R signaling. The agonists are known to activate NF-κB and mitogen-activated protein kinases to induce various proinflammatory mediators.[3] Binding of the IL-36R agonists to IL-1Rrp2 recruits IL-1RAcP, activating the signaling pathway. IL-36Ra binds to IL-36R, preventing the recruitment of IL-1RAcP.[1]

It has been found to activate T cell proliferation and release of IL-2.[4] Before the functions of the IL-36 cytokines were determined, they were named as derivatives of IL-1F; they were renamed to their current designations in 2010.[5] The genes encoding for the IL-36 cytokines are found on chromosome 2q13.[1]

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.[6] IL-36 has also been linked to psoriatic arthritis, systemic lupus erythematosus, inflammatory bowel disease, ulcerative colitis, Crohn's disease, and Sjögren's syndrome.[1]

IL-36 must be cleaved at the N-terminus to become active, but the enzyme responsible for this is not known.[5]

IL-36 is expressed by many cells types, most predominately keratinocytes, respiratory epithelium, various nervous tissue, and monocytes.[5][1]

References[]

  1. ^ a b c d e Ding L, Wang X, Hong X, Lu L, Liu D (January 2018). "IL-36 cytokines in autoimmunity and inflammatory disease". Oncotarget. 9 (2): 2895–2901. doi:10.18632/oncotarget.22814. PMC 5788690. PMID 29416822.
  2. ^ Zhou L, Todorovic V, Kakavas S, Sielaff B, Medina L, Wang L, Sadhukhan R, Stockmann H, Richardson PL, DiGiammarino E, Sun C, Scott V (January 2018). "Quantitative ligand and receptor binding studies reveal the mechanism of interleukin-36 (IL-36) pathway activation". The Journal of Biological Chemistry. 293 (2): 403–411. doi:10.1074/jbc.M117.805739. PMC 5767850. PMID 29180446.
  3. ^ 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". The Journal of Biological Chemistry. 286 (49): 42594–602. doi:10.1074/jbc.M111.267922. PMC 3234937. PMID 21965679.
  4. ^ 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.
  5. ^ a b c 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.
  6. ^ 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.
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