IL-36 in chronic inflammation and cancer |
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| Institution: | 1. Medical Clinic 1, Department of Medicine, University Hospital Erlangen, University of Erlangen-Nuremberg, Erlangen, Germany;2. Deutsches Zentrum Immuntherapie (DZI), Erlangen, Ulmenweg 18, 91054 Germany;1. Department of Pediatrics, First Peoples Hospital of Shangqiu City, Shangqiu 476000, Henan, PR China;2. Department of Chinese Medicine, Children Hospital of Kaifeng, Kaifeng 475000, Henan, PR China;3. Department of Pediatrics, Third Peoples‘ Hospital of Henan, Zhengzhou 476000, PR China;4. Department of Pediatrics, Peoples Hospital of Zhengzhou, Zhengzhou 476000, Henan, PR China;1. Department of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun, China;2. Department of Neurobiology, Care Sciences and Society, Karolinska Institute, Stockholm, Sweden;1. School of Veterinary Medicine and Science, University of Nottingham, UK;2. The Institute of Infection, Immunity and Inflammation, University of Nottingham, UK;1. Department of Dermatology, First Affiliated Hospital of Nanjing Medical University, Nanjing, China;2. Deparment of Dermatology, Zhenjiang First People’s Hospital, Zhenjiang, China;1. Department of Dermatology, University of Michigan, Ann Arbor, Mich;2. Department of Rheumatology, University of Michigan, Ann Arbor, Mich;3. Department of Pathology, University of Michigan, Ann Arbor, Mich;4. Department of Dermatology, First Affiliated Hospital of Nanjing Medical University, Nanjing, China |
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| Abstract: | IL-36 belongs to the IL-1 family of cytokines and activates target cells by binding to a specific cytokine receptor (IL-36R) followed by activation of intracellular regulators such as MAP kinases and NF-kappaB. Three subforms of IL-36, denoted IL-36alpha, IL-36beta and IL-36gamma, have been described that require N-terminal cleavage for activation. Functional studies have shown that IL-36 may activate a broad spectrum of immune and non-immune cells such as macrophages, T cells, keratinocytes and epithelial cells in an IL-1-independent fashion and thereby controls various inflammatory or oncogenic processes in the skin, the lung, the kidney, the liver and the intestine, respectively. Based on the presence of mutations of the IL-36RN in patients with generalized pustular psoriasis, successful clinical pilot trials with IL-36R blocking antibodies were conducted in these patients and further studies in patients with autoimmune or chronic inflammatory disorders such as inflammatory bowel diseases are under way. Collectively, these findings highlight a crucial regulatory role of IL-36 signaling in driving various inflammatory disorders that provide a rational basis for clinical targeting of this cytokine. |
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| Keywords: | Cytokines IL-36 Immune cells Inflammation |
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