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Advances in Mast Cell Activation by IL-1 and IL-33 in Sjögren’s Syndrome: Promising Inhibitory Effect of IL-37

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Postgraduate Medical School, University of Chieti, 66013 Chieti, Italy
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Department of Medicine and Science of Ageing, University of Chieti, 66013 Chieti, Italy
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School of Pharmacy, University of Camerino, 62032 Camerino, Italy
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Department of Biomedical Sciences and Specialist Surgery, Section of Ophthalmology, University of Ferrara, 44121 Ferrara, Italy
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University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA 19104, USA
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Department of Microbiology, University of Thessaloniki, 54124 Thessaloniki, Greece
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School of Veterinary Medicine, University of Thessaloniki, 54124 Thessaloniki, Greece
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Centro Medico “Mai più Dolore”, 65100 Pescara, Italy
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Maxillofacial Surgery “G. azzini” Hospital, 64100 Teramo, Italy
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Fondazione Policlinico Universitario A. Gemelli IRCCS, Università Cattolica del Sacro Cuore, 00100 Roma, Italy
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2020, 21(12), 4297; https://doi.org/10.3390/ijms21124297
Received: 13 May 2020 / Revised: 8 June 2020 / Accepted: 12 June 2020 / Published: 16 June 2020
Sjögren’s syndrome (SS) is a chronic autoimmune inflammatory disease that affects primarily older women and is characterized by irreversible damage of the exocrine glands, including tear (xerophthalmia) and salivary glands (xerostomia). Secretory glands lose their functionality due to the infiltration of immune cells, which produce cytokines and cause inflammation. Primary SS is characterized by dry syndrome with or without systemic commitment in the absence of other pathologies. Secondary SS is accompanied by other autoimmune diseases with high activation of B lymphocytes and the production of autoantibodies, including the rheumatoid factor. Other cells, such as CD4+ T cells and mast cells (MCs), participate in SS inflammation. MCs are ubiquitous, but are primarily located close to blood vessels and nerves and can be activated early in autoimmune diseases to express a wide variety of cytokines and chemokines. In the SS acute phase, MCs react by generating chemical mediators of inflammation, tumor necrosis factor (TNF), and other pro-inflammatory cytokines such as interleukin (IL)-1 and IL-33. IL-33 is the specific ligand for ST2 capable of inducing some adaptive immunity TH2 cytokines but also has pro-inflammatory properties. IL-33 causes impressive pathological changes and inflammatory cell infiltration. IL-1 family members can have paracrine and autocrine effects by exacerbating autoimmune inflammation. IL-37 is an IL-1 family cytokine that binds IL-18Rα receptor and/or Toll-like Receptor (TLR)4, exerting an anti-inflammatory action. IL-37 is a natural inhibitor of innate and acquired immunity, and the level is abnormal in patients with autoimmune disorders. After TLR ligand activation, IL-37 mRNA is generated in the cytoplasm, with the production of pro-IL-37 and later mature IL-37 caspase-1 mediated; both precursor and mature IL-37 are biologically active. Here, we discuss, for the first time, the current knowledge of IL-37 in autoimmune disease SS and propose a new therapeutic role. View Full-Text
Keywords: mast cell; Sjögren syndrome; IL-1; IL-33; inflammation; cytokine; immunity mast cell; Sjögren syndrome; IL-1; IL-33; inflammation; cytokine; immunity
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Conti, P.; Stellin, L.; Caraffa, A.; Gallenga, C.E.; Ross, R.; Kritas, S.K.; Frydas, I.; Younes, A.; Di Emidio, P.; Ronconi, G. Advances in Mast Cell Activation by IL-1 and IL-33 in Sjögren’s Syndrome: Promising Inhibitory Effect of IL-37. Int. J. Mol. Sci. 2020, 21, 4297.

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