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IL-33/IL-31 Axis in Immune-Mediated and Allergic Diseases
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IL-33/IL-31 Axis in Osteoporosis

1
Department of Life, Health and Environmental Sciences, University of L’Aquila, 67100 L’Aquila, Italy
2
Allergy and Clinical Immunology Unit, Center for the Diagnosis and Treatment of Osteoporosis, AUSL 04 64100 Teramo, Italy
3
Department of Dermatology, Hôpital Erasme, Université Libre de Bruxelles, 1070 Brussels, Belgium
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2020, 21(4), 1239; https://doi.org/10.3390/ijms21041239
Received: 8 January 2020 / Revised: 8 February 2020 / Accepted: 11 February 2020 / Published: 13 February 2020
(This article belongs to the Special Issue “IL-33/IL-31 Axis” in Allergic and Immune-Mediated Diseases)
The study of the immunoskeletal interface has led to the discovery of numerous cytokines involved in the regulation of bone remodeling, providing valuable information on the pathogenesis of osteoporosis. The role of inflammatory cytokines of the Th1 and Th17 profile in osteoporosis is well known. Here we focus on two newly discovered Th2 cytokines, IL-31 and IL-33, whose implications in osteoporosis are recently emerging. Clinical and experimental observations suggest an important role of the IL-33/IL-31 axis in osteoporosis. IL-33 induces IL-31 secretion by Th2 cells and inhibits RANKL-dependent osteoclastogenesis, thus counteracting bone loss. IL-31 influences Th1/Th17 osteoclastogenetic inflammation and limits Th2 osteoprotective processes, thus favoring osteoporosis. Better knowledge of the role of IL-31 and IL-33 and their receptor complexes in osteoporosis could provide an interesting perspective for the development of new and more effective therapies, possibly with less side effects. View Full-Text
Keywords: osteoporosis; IL-31; IL-33; bone; osteoimmunology; immunity; allergy osteoporosis; IL-31; IL-33; bone; osteoimmunology; immunity; allergy
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De Martinis, M.; Sirufo, M.M.; Suppa, M.; Ginaldi, L. IL-33/IL-31 Axis in Osteoporosis. Int. J. Mol. Sci. 2020, 21, 1239.

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