Regulation and function of interleukin-36 cytokines.
Autor: | Bassoy EY; Division of Rheumatology, Department of Internal Medicine Specialties & Department of Pathology-Immunology, University Hospitals of Geneva and University of Geneva, Geneva, Switzerland., Towne JE; Immunology Discovery, Janssen Research and Development, San Diego, CA, USA., Gabay C; Division of Rheumatology, Department of Internal Medicine Specialties & Department of Pathology-Immunology, University Hospitals of Geneva and University of Geneva, Geneva, Switzerland. |
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Jazyk: | angličtina |
Zdroj: | Immunological reviews [Immunol Rev] 2018 Jan; Vol. 281 (1), pp. 169-178. |
DOI: | 10.1111/imr.12610 |
Abstrakt: | The interleukin (IL)-36 cytokines include 3 agonists, IL-36α, IL-36β, and IL-36γ that bind to a common receptor composed of IL-36R and IL-1RAcP to stimulate inflammatory responses. IL-36Ra is a natural antagonist that binds to IL-36R, but does not recruit the co-receptor IL-1RAcP and does not stimulate any intracellular responses. The IL-36 cytokines are expressed predominantly by epithelial cells and act on a number of cells including immune cells, epithelial cells, and fibroblasts. Processing of the N-terminus is required for full agonist or antagonist activity for all IL-36 members. The role of IL-36 has been extensively demonstrated in the skin where it can act on keratinocytes and immune cells to induce a robust inflammatory response that has been implicated in psoriatic disorders. Emerging data also suggest a role for this cytokine family in pulmonary and intestinal physiology and pathology. (© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.) |
Databáze: | MEDLINE |
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