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DOI: 10.1615/CritRevImmunol.2020033176
pages 267-274

Mast Cells Mediate Rheumatoid Arthritis−Inhibitory Role of IL-37

Pio Conti
Postgraduate Medical School, University of Chieti, Chieti, Italy
Dorina Lauritano
Medicine and Surgery Department, Centre of Neuroscience of Milan, University of Milan-Bicocca, Italy
Alessandro Caraffa
School of Pharmacy, University of Camerino, Camerino, Italy
Carla E. Gallenga
Department of Biomedical Sciences and Specialist Surgery, Section of Ophthalmology, University of Ferrara, Ferrara, Italy
Francesco Carinci
Department of Morphology, Surgery and Experimental Medicine, University of Ferrara, Ferrara, Italy
Gianpaolo Ronconi
Clinica dei Pazienti del Territorio, Policlinico Gemelli, Roma, Italy
Spiros K. Kritas
Department of Microbiology, University of Thessaloniki, Thessaloniki, Greece
Paolo Di Emidio
Maxillofacial Surgery "G. Mazzini" Hospital, Teramo, Italy
Stefano Martinotti
Unit of Molecular Biology and Predictive Medicine, Department of Medical, Oral and Biotechnological Science, University of Chiet-Pescara, Chieti, Italy
Franco Pandolfi
Immunology and Allergology Department, Fondazione Policlinico Universitario A. Gemelli IRCCS, Università Cattolica del Sacro Cuore, Roma, Italy

ABSTRACT

Rheumatoid arthritis (RA) is an autoimmune, chronic inflammatory, disabling arthropathy that severely affects the quality of life. This disease involves several proinflammatory cytokines, including interleukin (IL)-1β and tumor necrosis factor (TNF). IL-1 induces TNF and vice versa, causing joint damage and cartilage degradation. Current antirheumatic drugs may be effective, but they possess many unwanted side effects. In recent years, inhibitors of proinflammatory cytokines have increasingly entered mainstream clinical practice. Recent evidence indicates that IL-37, which has anti-inflammatory properties, is increased in the serum and is released from white blood cells in patients with RA. Mast cells (MCs), stimulated by the neuropeptide substance P (SP) and IL-33, release IL-1β and TNF. Recent evidence indicates that large amounts of IL-1β and TNF can be released from human MCs, which also secrete CXCL8, which promotes migration of immune cells, causing erosion of the bone and cartilage. Treatment with IL-37 can block the MC stimulation and release of inflammatory compounds, attenuating the severity of the disease and/or altering its progression.

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