{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,10]],"date-time":"2026-02-10T17:23:09Z","timestamp":1770744189320,"version":"3.49.0"},"reference-count":60,"publisher":"Oxford University Press (OUP)","issue":"9","license":[{"start":{"date-parts":[[2017,5,1]],"date-time":"2017-05-01T00:00:00Z","timestamp":1493596800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2017,5,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Inflammatory bone resorption mediated by osteoclasts is a major cause of morbidity and disability in many inflammatory disorders, including rheumatoid arthritis (RA). The mechanisms that regulate osteoclastogenesis and bone resorption in inflammatory settings are complex and have not been well elucidated. In this study, we identify the immunoregulator differentially expressed in FDCP 6 homolog (Def6) as a novel inhibitor of osteoclastogenesis in physiological and inflammatory conditions. Def6 deficiency in Def6\u2212\/\u2212 mice enhanced the sensitivity of osteoclast precursors to the physiological osteoclastogenic inducer receptor activator for NF-\u03baB ligand, and Def6\u2212\/\u2212 osteoclasts formed actin rings. Furthermore, Def6 deficiency markedly increased TNF-\u03b1\u2013induced osteoclastogenesis in vitro and in vivo and enhanced bone resorption in an inflammatory osteolysis mouse model. TNF-\u03b1 serum levels correlated negatively with Def6 expression levels in osteoclast precursors obtained from RA patients, and the osteoclastogenic capacity of the osteoclast precursors was significantly inversely correlated with their Def6 expression levels, indicating that Def6 functions as an inhibitor of excessive osteoclast formation and bone destruction in RA. Mechanistically, Def6 suppressed osteoclastogenesis and the expression of key osteoclastogenic factors NFATc1, B lymphocyte\u2013induced maturation protein-1, and c-Fos by regulating an endogenous IFN-\u03b2\u2013mediated autocrine feedback loop. The Def6-dependent pathway may represent a novel therapeutic target to prevent pathological bone destruction.<\/jats:p>","DOI":"10.4049\/jimmunol.1601716","type":"journal-article","created":{"date-parts":[[2017,3,18]],"date-time":"2017-03-18T03:00:17Z","timestamp":1489806017000},"page":"3436-3447","source":"Crossref","is-referenced-by-count":16,"title":["Def6 Restrains Osteoclastogenesis and Inflammatory Bone Resorption"],"prefix":"10.1093","volume":"198","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1237-8102","authenticated-orcid":false,"given":"Nikolaus","family":"Binder","sequence":"first","affiliation":[{"name":"Arthritis and Tissue Degeneration Program and The David Z. 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