title: Interleukin-10 and articular cartilage: experimental therapeutical approaches in cartilage disorders.
abstract: Interleukin (IL)-10 is a well known anti-inflammatory and immunoregulatory cytokine, mainly released by, and acting on cells of the immune system such as monocytes, macrophages, T cells, NK cells, and B cells. IL-10 is also produced by a few connective tissue cell types including chondrocytes and is involved in processes such as connective tissue extracellular matrix remodelling, although it's exact function in articular cartilage remains unclear. This review article summarizes after a short insight into functions of IL-10 in the immune system most of the published literature on the role of IL-10 in articular cartilage homeostasis and disorders. A critical analysis of the present literature was undertaken leading to a survey of the significance of IL-10 in rheumatoid arthritis (RA), osteoarthritis (OA) and blood induced cartilage damage with particular focus on the direct impact of IL-10 on chondrocyte biology. IL-10 is up-regulated in RA and OA and therapeutic effects of IL-10 in experimental arthritis using several gene therapeutic approaches were reported, mainly through an immune cell mediated immunosuppression mechanism. Recently, a direct anti-inflammatory, -catabolic and -apoptotic potential of IL-10 in cartilage was described, suggesting a chondroprotective effect of IL-10, not only in RA and OA, but also in non-RA and non-systemic cartilage disorders. Chondroprotection by IL-10 may be a promising tool in arthritis therapy, as IL-10 plays a role in joint and cartilage immunoregulation and homeostasis. However, a crucial problem remains to be the optimisation of local and continuous therapeutic effective levels of IL-10 administration in the joint.
authors.affiliation: Department for Trauma and Reconstructive Surgery, Charité-University of Medicine, Campus Benjamin Franklin, Berlin, Germany. gundula.schulze-tanzil@charite.de
authors.forename: Gundula
authors.initials: G
authors.lastname: Schulze-Tanzil
authors.forename: Hala
authors.initials: H
authors.lastname: Zreiqat
authors.forename: Robert
authors.initials: R
authors.lastname: Sabat
authors.forename: Benjamin
authors.initials: B
authors.lastname: Kohl
authors.forename: Andreas
authors.initials: A
authors.lastname: Halder
authors.forename: Riccarda D
authors.initials: RD
authors.lastname: Müller
authors.forename: Thilo
authors.initials: T
authors.lastname: John
mesh_terms: D000818:Animals; D001169:Arthritis, Experimental / Q000628:therapy; D001172:Arthritis, Rheumatoid / Q000628:therapy*; D002357:Cartilage Diseases / Q000628:therapy*; D002358:Cartilage, Articular / Q000276:immunology* / Q000473:pathology; D019902:Chondrocytes / Q000276:immunology; D004195:Disease Models, Animal; D051547:Heme Oxygenase-1 / Q000235:genetics / Q000276:immunology; D006801:Humans; D016753:Interleukin-10 / Q000235:genetics* / Q000276:immunology*; D053583:Interleukin-1beta / Q000235:genetics / Q000276:immunology; D007596:Joints / Q000276:immunology / Q000473:pathology; D051379:Mice; D010003:Osteoarthritis / Q000628:therapy; D011817:Rabbits; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000276:immunology
chemical_list: D053583:Interleukin-1beta; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; C496541:HMOX1 protein, human; D051547:Heme Oxygenase-1