{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,12]],"date-time":"2026-06-12T22:42:45Z","timestamp":1781304165109,"version":"3.54.1"},"reference-count":30,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2023,6,10]],"date-time":"2023-06-10T00:00:00Z","timestamp":1686355200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,3,28]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n               <jats:sec>\n                  <jats:title>Objectives<\/jats:title>\n                  <jats:p>Decreased sialylation of IgG-Fc glycans has been reported in autoimmune diseases, but its role in systemic lupus erythematosus (SLE) is not fully understood. In this study, we examined the pathogenicity of IgG desialylation and its association with Th17 in SLE using an animal model.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>B6SKG mice, which develop lupus-like systemic autoimmunity due to the ZAP70 mutation, were used to investigate the pathogenicity of IgG desialylation. The proportion of sialylated IgG was compared between B6SKG and wild-type mice with or without \u03b2-glucan treatment-induced Th17 expansion. Anti-interleukin (IL)-23 and anti-IL-17 antibodies were used to examine the role of Th17 cells in IgG glycosylation. Activation-induced cytidine deaminase\u2013specific St6gal1 conditionally knockout (cKO) mice were generated to examine the direct effect of IgG desialylation.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>The proportions of sialylated IgG were similar between B6SKG and wild-type mice in the steady state. However, IgG desialylation was observed after \u03b2-glucan-induced Th17 expansion, and nephropathy also worsened in B6SKG mice. Anti-IL-23\/17 treatment suppressed IgG desialylation and nephropathy. Glomerular atrophy was observed in the cKO mice, suggesting that IgG desialylation is directly involved in disease exacerbation.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>IgG desialylation contributes to the progression of nephropathy, which is ameliorated by blocking IL-17A or IL-23 in an SLE mouse model.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/mr\/road054","type":"journal-article","created":{"date-parts":[[2023,6,10]],"date-time":"2023-06-10T15:13:10Z","timestamp":1686409990000},"page":"523-529","source":"Crossref","is-referenced-by-count":7,"title":["Pathogenicity of\u00a0IgG-Fc desialylation and\u00a0its association with Th17 cells in\u00a0an animal model of\u00a0systemic lupus erythematosus"],"prefix":"10.1093","volume":"34","author":[{"given":"Yuri","family":"Nishida","sequence":"first","affiliation":[{"name":"Department of Rheumatology and Clinical Immunology, Kyoto University Graduate School of Medicine , Kyoto, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mirei","family":"Shirakashi","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Clinical Immunology, Kyoto University Graduate School of Medicine , Kyoto, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Noritaka","family":"Hashii","sequence":"additional","affiliation":[{"name":"Division of Biological Chemistry and Biologicals, National Institute of Health Sciences , Kanagawa, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ran","family":"Nakashima","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Clinical Immunology, Kyoto University Graduate School of Medicine , Kyoto, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoichi","family":"Nakayama","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Clinical Immunology, Kyoto University Graduate School of Medicine , Kyoto, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masao","family":"Katsushima","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Clinical Immunology, Kyoto University Graduate School of Medicine , Kyoto, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ryu","family":"Watanabe","sequence":"additional","affiliation":[{"name":"Department of Clinical Immunology, Graduate School of Medicine, Osaka Metropolitan University , Osaka, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hideo","family":"Onizawa","sequence":"additional","affiliation":[{"name":"Department of Advanced Medicine for Rheumatic Diseases, Kyoto University Graduate School of Medicine , Kyoto, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ryosuke","family":"Hiwa","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Clinical Immunology, Kyoto University Graduate School of Medicine , Kyoto, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hideaki","family":"Tsuji","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Clinical Immunology, Kyoto University Graduate School of Medicine , Kyoto, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Koji","family":"Kitagori","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Clinical Immunology, Kyoto University Graduate School of Medicine , Kyoto, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuji","family":"Akizuki","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Clinical Immunology, Kyoto University Graduate School of Medicine , Kyoto, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akira","family":"Onishi","sequence":"additional","affiliation":[{"name":"Department of Advanced Medicine for Rheumatic Diseases, Kyoto University Graduate School of Medicine , Kyoto, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5981-4648","authenticated-orcid":false,"given":"Kosaku","family":"Murakami","sequence":"additional","affiliation":[{"name":"Center for Cancer Immunotherapy and Immunobiology, Graduate School of Medicine, Kyoto University , Kyoto, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7082-4900","authenticated-orcid":false,"given":"Hajime","family":"Yoshifuji","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Clinical Immunology, Kyoto University Graduate School of Medicine , Kyoto, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masao","family":"Tanaka","sequence":"additional","affiliation":[{"name":"Department of Advanced Medicine for Rheumatic Diseases, Kyoto University Graduate School of Medicine , Kyoto, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tatsuaki","family":"Tsuruyama","sequence":"additional","affiliation":[{"name":"Department of Drug Discovery Medicine, Graduate School of Medicine, Kyoto University , Kyoto, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akio","family":"Morinobu","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Clinical Immunology, Kyoto University Graduate School of Medicine , Kyoto, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Motomu","family":"Hashimoto","sequence":"additional","affiliation":[{"name":"Department of Clinical Immunology, Graduate School of Medicine, Osaka Metropolitan University , Osaka, 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