{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T01:37:59Z","timestamp":1792546679258,"version":"4.5.0"},"reference-count":75,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2013,9,5]],"date-time":"2013-09-05T00:00:00Z","timestamp":1378339200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Clin Investigation"],"published-print":{"date-parts":[[2013,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      The role of\n                      <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\n                      helper (Th) 17 cells in autoimmune diseases has been extensively studied recently, but its function in oestrogen\u2010deficient osteoporosis remains undefined. This review aimed to explore the role of Th17 cells in regulating bone loss induced by oestrogen deficiency.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and methods<\/jats:title>\n                    <jats:p>\n                      We searched PubMed, Embase, Google Scholar and Biosis up to 1\n                      <jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>\n                      ebruary 2013 for immune regulation of oestrogen\u2010deficient osteoporosis by Th17 cells. Terms relevant to immunity, oestrogen deficiency, osteoporosis and Th17 cells were used for database searching. Seventy\u2010five papers met the predetermined searching criteria.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Studies indicate Th17 lineage to be a potent osteoclastogenic mediator in oestrogen\u2010deficient osteoporosis. Oestrogen deficiency promotes osteoclastogenesis by up\u2010regulating Th17 cell populations in bone marrow and\n                      <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                      \u201017 levels in peripheral blood. Meanwhile, transcription factors involved in Th17 cell differentiation, such as\n                      <jats:styled-content style=\"fixed-case\">ROR<\/jats:styled-content>\n                      \u03b3t and\n                      <jats:styled-content style=\"fixed-case\">ROR<\/jats:styled-content>\n                      \u03b1, are highly expressed in ovariectomized animals. Treatment with\n                      <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                      \u201017 significantly promotes production of\n                      <jats:styled-content style=\"fixed-case\">RANKL<\/jats:styled-content>\n                      ,\n                      <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\n                      and\n                      <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                      \u20106 as well as\n                      <jats:styled-content style=\"fixed-case\">TRAP<\/jats:styled-content>\n                      <jats:sup>+<\/jats:sup>\n                      cells in culture; blocking\n                      <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                      \u201017 pathway significantly reduces abundance of Th17 cells and effectively prevents bone loss in ovariectomized mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      The main body of literatures suggests Th17 to be a critical modulator in the pathogenesis of oestrogen\u2010deficient osteoporosis, which supports the notion that oestrogen\u2010deficient osteoporosis is a complex interplay between oestrogen, osteoclastogenic cytokines and osteoclasts. In addition, therapeutic strategies targeting\n                      <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                      \u201017 networks may be clinically useful in treatment for postmenopausal osteoporosis.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/eci.12158","type":"journal-article","created":{"date-parts":[[2013,8,14]],"date-time":"2013-08-14T03:57:29Z","timestamp":1376452649000},"page":"1195-1202","source":"Crossref","is-referenced-by-count":55,"title":["Immune regulation of bone loss by\n                    <scp>T<\/scp>\n                    h17 cells in oestrogen\u2010deficient osteoporosis"],"prefix":"10.1111","volume":"43","author":[{"given":"Renqing","family":"Zhao","sequence":"first","affiliation":[{"name":"College of Physical Education and Health Sciences Zhejiang Normal University Jinhua Zhejiang 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