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In animals, PHPT is modeled by continuous PTH treatment (cPTH). In mice, an additional critical action of cPTH is the capacity to increase the production of RANKL by osteocytes. However, a definitive link between IL-17A and osteocytic expression of RANKL has not been made. Here we show that cPTH fails to induce cortical and trabecular bone loss and causes less intense bone resorption in conditional knock-out (IL-17RA\u0394OCY) male and female mice lacking the expression of IL-17A receptor (IL-17RA) in dentin matrix protein 1 (DMP1)-8kb-Cre\u2013expressing cells, which include osteocytes and some osteoblasts. Therefore, direct IL-17RA signaling in osteoblasts\/osteocytes is required for cPTH to exert its bone catabolic effects. In addition, in vivo, silencing of IL-17RA signaling in in DMP1-8kb\u2013expressing cells blunts the capacity of cPTH to stimulate osteocytic RANKL production, indicating that cPTH augments osteocytic RANKL expression indirectly, via an IL-17A\/IL-17RA\u2013mediated mechanism. Thus, osteocytic production of RANKL and T cell production of IL-17A are both critical for the bone catabolic activity of cPTH. \u00a9 2018 American Society for Bone and Mineral Research.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1002\/jbmr.3600","type":"journal-article","created":{"date-parts":[[2018,11,6]],"date-time":"2018-11-06T19:19:12Z","timestamp":1541531952000},"page":"349-360","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":77,"title":["IL-17 Receptor Signaling in Osteoblasts\/Osteocytes Mediates PTH-Induced Bone Loss and Enhances Osteocytic RANKL Production"],"prefix":"10.1093","volume":"34","author":[{"given":"Jau-Yi","family":"Li","sequence":"first","affiliation":[{"name":"Division of EndocrinologyMetabolism and LipidsDepartment of MedicineEmory UniversityAtlantaGAUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mingcan","family":"Yu","sequence":"additional","affiliation":[{"name":"Division of EndocrinologyMetabolism and LipidsDepartment of MedicineEmory UniversityAtlantaGAUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abdul Malik","family":"Tyagi","sequence":"additional","affiliation":[{"name":"Division of EndocrinologyMetabolism and LipidsDepartment of MedicineEmory UniversityAtlantaGAUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chiara","family":"Vaccaro","sequence":"additional","affiliation":[{"name":"Division of EndocrinologyMetabolism and LipidsDepartment of MedicineEmory UniversityAtlantaGAUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emory","family":"Hsu","sequence":"additional","affiliation":[{"name":"Division of EndocrinologyMetabolism and LipidsDepartment of MedicineEmory 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