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485-517, 2009."},{"key":"9","unstructured":"9) Sato, K., et al.: Th17 functions as an osteoclastogenic helper T cell subset that links T cell activation and bone destruction. <i>The Journal of experimental medicine<\/i>. <b>203<\/b>: 2673-2682, 2006."},{"key":"10","unstructured":"10) Okamoto, K., Takayanagi, H.: Regulation of bone by the adaptive immune system in arthritis. <i>Arthritis Res Ther<\/i>. <b>13<\/b>: 219, 2011."},{"key":"11","unstructured":"11) Komatsu, N., et al.: Pathogenic conversion of Foxp3<sup>+<\/sup> T cells into T<sub>H<\/sub>17 cells in autoimmune arthritis. <i>Nat Med<\/i>. <b>20<\/b>: 62-68, 2014."},{"key":"12","unstructured":"12) Guerrini, M.M., et al.: Inhibition of the TNF Family Cytokine RANKL Prevents Autoimmune Inflammation in the Central Nervous System. <i>Immunity<\/i>. <b>43<\/b>: 1174-1185, 2015."},{"key":"13","unstructured":"13) Negishi-Koga, T., et al.: Immune complexes regulate bone metabolism through FcR\u03b3 signalling. <i>Nature communications<\/i>. <b>6<\/b>: 6637, 2015."},{"key":"14","unstructured":"14) Harre, U., et al.: Glycosylation of immunoglobulin G determines osteoclast differentiation and bone loss. <i>Nature communications.<\/i> <b>6<\/b>: 6651, 2015."},{"key":"15","unstructured":"15) Pfeifle, R., et al.: Regulation of autoantibody activity by the IL-23-T<sub>H<\/sub>17 axis determines the onset of autoimmune disease. <i>Nature immunology<\/i>. <b>18<\/b>: 104-113, 2017."},{"key":"16","unstructured":"16) Sherlock, J.P., et al.: IL-23 induces spondyloarthropathy by acting on ROR-\u03b3t+ CD3<sup>+<\/sup>CD4<sup>\u2212<\/sup>CD8<sup>\u2212<\/sup> entheseal resident T cells. <i>Nat Med<\/i>. <b>18<\/b>: 1069-1076, 2012."},{"key":"17","unstructured":"17) Ciccia, F., et al.: Type 3 innate lymphoid cells producing IL-17 and IL-22 are expanded in the gut, in the peripheral blood, synovial fluid and bone marrow of patients with ankylosing spondylitis. <i>Ann Rheum Dis<\/i>. <b>74<\/b>: 1739-1747, 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