{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,10]],"date-time":"2026-10-10T00:08:36Z","timestamp":1791590916445,"version":"4.3.4"},"reference-count":66,"publisher":"Oxford University Press (OUP)","issue":"9","license":[{"start":{"date-parts":[[2014,3,28]],"date-time":"2014-03-28T00:00:00Z","timestamp":1395964800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2014,9,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n               <jats:sec>\n                  <jats:title>\u2003<\/jats:title>\n                  <jats:p>Activated T cell has a key role in the interaction between bone and immune system. T cells produce proinflammatory cytokines, including receptor activator of NF-\u03baB ligand (RANKL), tumor necrosis factor \u03b1 (TNF-\u03b1), and interleukin 17 (IL-17), all of which augment osteoclastogenesis. RANKL and TNF-\u03b1 are targeted by inhibitors such as denosumab, a human monoclonal RANKL antibody, and infliximab, which neutralizes TNF-\u03b1. IL-17 is also an important mediator of bone loss, and an antibody against IL-17 is undergoing phase II clinical trial for rheumatoid arthritis. Although there are a few studies showing suppression of Th17 cell differentiation and induction of regulatory T cells (Tregs) by infliximab, the effect of denosumab remains poorly understood. In this study, we investigated the effects of anti-TNF-\u03b1, anti-RANKL, or anti-IL-17 antibody administration to estrogen-deficient mice on CD4+ T-cell proliferation, CD28 loss, Th17\/Treg balance and B lymphopoesis, and finally, the translation of these immunomodulatory effects on skeletal parameters. Adult Balb\/c mice were treated with anti-RANKL\/-TNF-\u03b1\/-IL-17 subcutaneously, twice a week, postovariectomy (Ovx) for 4 weeks. Animals were then autopsied; bone marrow cells were collected for FACS and RNA analysis and serum collected for ELISA. Bones were dissected for static and dynamic histomorphometry studies. We observed that although anti-RANKL and anti-TNF-\u03b1 therapies had no effect on Ovx-induced CD4+ T-cell proliferation and B lymphopoesis, anti-IL-17 effectively suppressed both events with concomitant reversal of CD28 loss. Anti-IL-17 antibody reduced proinflammatory cytokine production and induced Tregs. All three antibodies restored trabecular microarchitecture with comparable efficacy; however, cortical bone parameters, bone biomechanical properties, and histomorphometry were best preserved by anti-IL-17 antibody, likely attributable to its inhibitory effect on osteoblast apoptosis and increased number of bone lining cells and Wnt10b expression. Based on the superior immunoprotective effects of anti-IL-17, which appears to translate to a better skeletal preservation, we propose beginning clinical trials using a humanized antibody against IL-17 for treatment of postmenopausal osteoporosis. \u00a9 2014 American Society for Bone and Mineral Research.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1002\/jbmr.2228","type":"journal-article","created":{"date-parts":[[2014,3,28]],"date-time":"2014-03-28T21:12:04Z","timestamp":1396041124000},"page":"1981-1992","source":"Crossref","is-referenced-by-count":114,"title":["Enhanced Immunoprotective Effects by Anti-IL-17 Antibody Translates to Improved Skeletal Parameters Under Estrogen Deficiency Compared With Anti-RANKL and Anti-TNF-\u03b1 Antibodies"],"prefix":"10.1093","volume":"29","author":[{"given":"Abdul M","family":"Tyagi","sequence":"first","affiliation":[{"name":"Division of Endocrinology and Centre for Research in Anabolic Skeletal Targets in Health and Illness (ASTHI)CSIR-Central Drug Research InstituteLucknowIndia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohd N","family":"Mansoori","sequence":"additional","affiliation":[{"name":"Division of Endocrinology and Centre for Research in Anabolic Skeletal Targets in Health and Illness (ASTHI)CSIR-Central Drug Research InstituteLucknowIndia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kamini","family":"Srivastava","sequence":"additional","affiliation":[{"name":"Division of Endocrinology and Centre for Research in Anabolic Skeletal Targets in Health and Illness (ASTHI)CSIR-Central Drug Research InstituteLucknowIndia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohd P","family":"Khan","sequence":"additional","affiliation":[{"name":"Division of Endocrinology and Centre for Research in Anabolic Skeletal Targets in Health and Illness (ASTHI)CSIR-Central Drug Research InstituteLucknowIndia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jyoti","family":"Kureel","sequence":"additional","affiliation":[{"name":"Division of Endocrinology and Centre for Research in Anabolic Skeletal Targets in Health and Illness (ASTHI)CSIR-Central Drug Research InstituteLucknowIndia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Manisha","family":"Dixit","sequence":"additional","affiliation":[{"name":"Division of Endocrinology and Centre for Research in Anabolic Skeletal Targets in Health and Illness (ASTHI)CSIR-Central Drug Research InstituteLucknowIndia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Priyanka","family":"Shukla","sequence":"additional","affiliation":[{"name":"Division of Endocrinology and Centre for Research in Anabolic Skeletal Targets in Health and Illness (ASTHI)CSIR-Central Drug Research 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