{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,26]],"date-time":"2026-02-26T15:03:29Z","timestamp":1772118209324,"version":"3.50.1"},"reference-count":46,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2024,4,2]],"date-time":"2024-04-02T00:00:00Z","timestamp":1712016000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["acrjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Arthritis &amp; Rheumatology"],"published-print":{"date-parts":[[2024,7]]},"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Interleukin\u201023 (IL\u201023) is a crucial cytokine implicated in chronic inflammation and autoimmunity, associated with various diseases such as psoriasis, psoriatic arthritis, and systemic lupus erythematosus (SLE). This study aimed to create and characterize a transgenic mouse model overexpressing human IL\u201023A (TghIL\u201023A), providing a valuable tool for investigating the pathogenic role of human IL\u201023A and evaluating the efficacy of anti\u2013human IL\u201023A therapeutics.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      TghIL\u201023A mice were generated via microinjection of CBA \u00d7 C57BL\/6 zygotes with a fragment of the human\n                      <jats:italic>IL23A<\/jats:italic>\n                      gene, flanked by its 5\u2032\u2010regulatory sequences and the 3\u2032 untranslated region of human \u03b2\u2010globin. The TghIL\u201023A pathology was assessed through hematologic and biochemic analyses, cytokine and antinuclear antibody detection, and histopathologic examination of skin and renal tissues. The response to the anti\u2013human IL\u201023A therapeutic agent guselkumab was evaluated in groups of eight mixed\u2010sex mice receiving subcutaneous treatment twice weekly for 10 weeks using clinical, biomarker, and histopathologic readouts.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>TghIL\u201023A mice exhibited interactions between human IL\u201023A and mouse IL\u201023\/IL\u201012p40 and developed a chronic multiorgan autoimmune disease marked by proteinuria, anti\u2013double\u2010stranded DNA antibodies, severe inflammatory lesions in the skin, and milder phenotypes in the kidneys and lungs. The TghIL\u201023A pathologic features exhibited significant similarities to those observed in human patients with SLE, and they were reversed following guselkumab treatment.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>We have generated and characterized a novel genetic mouse model of SLE, providing proof\u2010of\u2010concept for the etiopathogenic role of human IL\u201023A. This new model has a normal life span and integrates several characteristics of the human disease's complexity and chronicity, making it an attractive preclinical tool for studying IL\u201023\u2013dependent pathogenic mechanisms and assessing the efficacy of anti\u2013human IL\u201023A or modeled disease\u2010related therapeutics.<\/jats:p>\n                    <jats:p>\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/art42830-toc-0001-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                    <\/jats:p>\n                  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