{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T10:36:05Z","timestamp":1788777365589,"version":"build-2803163510"},"reference-count":53,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2025,12,30]],"date-time":"2025-12-30T00:00:00Z","timestamp":1767052800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2025,12,30]],"date-time":"2025-12-30T00:00:00Z","timestamp":1767052800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100008897","name":"Janssen Pharmaceutica","doi-asserted-by":"publisher","award":["430070383"],"award-info":[{"award-number":["430070383"]}],"id":[{"id":"10.13039\/100008897","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["P01AI179405"],"award-info":[{"award-number":["P01AI179405"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["acrjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Arthritis &amp; Rheumatology"],"published-print":{"date-parts":[[2026,3]]},"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Up\u2010regulation of interleukin\u201023 (IL\u201023) in the serum and kidneys of patients with lupus nephritis (LN) has been demonstrated, but its effect on podocytes remains unknown. We hypothesized that IL\u201023 contributes to podocyte injury and that targeted deletion of IL\u201023 receptor (IL\u201023R) in podocytes of lupus\u2010prone mice can prevent the development of glomerulonephritis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Kidney biopsies were immunostained for IL\u201023R. In vitro experiments were conducted using a human podocyte cell line and primary murine podocytes. Human podocytes stimulated with IL\u201023 underwent bulk RNA sequencing. The expression of IL\u201023R and structure and motility of podocytes were assessed. Podocytes isolated from B6 wild\u2010type mice injected with a minicircle (MC) encoding IL\u201023 were studied. To assess the role of IL\u201023R in the development of nephritis, we generated MRL\/\n                      <jats:italic>lpr<\/jats:italic>\n                      mice deficient in podocyte\u2010specific\n                      <jats:italic>Il23r<\/jats:italic>\n                      who were lupus prone.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      IL\u201023R was highly expressed in the glomeruli of patients with LN. IL\u201023R expression was also up\u2010regulated in human podocytes and primary podocytes isolated from B6 mice after IL\u201023 stimulation. Human podocytes stimulated with IL\u201023 showed decreased expression of synaptopodin and remodeling of the actin cytoskeleton. Mice who were administered with IL\u201023 MC mice exhibited a significant increase in the expression of IL\u201023R and phosphorylated STAT3 in podocytes. Finally, MRL\/\n                      <jats:italic>lpr<\/jats:italic>\n                      .Podo\u2010Cre\n                      <jats:sup>+<\/jats:sup>\n                      <jats:italic>Il23r<\/jats:italic>\n                      <jats:sup>fl\/fl<\/jats:sup>\n                      mice showed decreased clinical and histologic features of LN.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      IL\u201023R expression is increased in podocytes from mice and humans with systemic lupus erythematosus. IL\u201023 signaling disrupts the cytoskeleton in podocytes and increases their mobility, leading to the development of glomerulonephritis. Podocyte\u2010specific deletion of\n                      <jats:italic>Il23r<\/jats:italic>\n                      in lupus\u2010prone mice abrogates the development of LN.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/art.43395","type":"journal-article","created":{"date-parts":[[2025,9,15]],"date-time":"2025-09-15T08:46:38Z","timestamp":1757925998000},"page":"672-683","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Podocyte Interleukin\u201023 Receptor Signaling in the Pathogenesis of Lupus Nephritis"],"prefix":"10.1002","volume":"78","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9240-0359","authenticated-orcid":false,"given":"Rong","family":"Fu","sequence":"first","affiliation":[{"name":"Department of Medicine, Beth Israel Deaconess Medical Center Harvard Medical School  Boston 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