{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T20:43:18Z","timestamp":1791492198464,"version":"4.3.4"},"reference-count":37,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2025,10,15]],"date-time":"2025-10-15T00:00:00Z","timestamp":1760486400000},"content-version":"vor","delay-in-days":14,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100002336","name":"Daiichi Sankyo Company","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100002336","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Nephrology"],"published-print":{"date-parts":[[2025,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aim<\/jats:title>\n                    <jats:p>IgA nephropathy (IgAN) is the most common primary glomerulonephritis worldwide, yet its pathogenesis remains incompletely understood. B cell activating factor (BAFF), a TNF family member involved in B cell activation and IgA class switching, has been proposed as a potential pathogenic factor in IgAN. However, its role in disease progression is unclear. This study aimed to investigate the pathological role of BAFF in IgAN using grouped ddY (gddY) mice, a spontaneous murine model of IgAN.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>gddY mice were treated with anti\u2010BAFF monoclonal antibody (anti\u2010BAFF Ab) or PBS via intraperitoneal injection twice a week for 4\u2009weeks. Urinary albumin, serum immunoglobulins, and IgA\u2010IgG immune complex were measured pre\u2010 and post\u2010treatment. Serum levels of aberrantly glycosylated IgA were quantified using specific lectin\u2010based assays. Glomerular IgA and C3 depositions were evaluated by immunofluorescence, and B cell populations in spleen and bone marrow were analysed by flowcytometry.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Anti\u2010BAFF Ab treatment significantly reduced serum IgA, IgG, and IgM levels as compared with PBS treatment (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.003, and\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.002, respectively). However, it did not affect serum aberrantly glycosylated IgA, IgA\u2010IgG immune complex, and urinary albumin excretion. Glomerular depositions of IgA and C3 as well as B cell population in the spleen and bone marrow were also not affected by anti\u2010BAFF Ab treatment.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>BAFF inhibition reduces general immunoglobulin levels but does not impact nephritogenic IgA production or disease progression in murine IgAN. These findings suggest that BAFF\u2010dependent IgA production may not be involved in the pathogenesis of IgAN.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/nep.70139","type":"journal-article","created":{"date-parts":[[2025,10,16]],"date-time":"2025-10-16T00:39:43Z","timestamp":1760575183000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["B Cell Activating Factor Does Not Play a Pivotal Role in the Synthesis of Aberrantly Glycosylated\n                    <scp>IgA<\/scp>"],"prefix":"10.1111","volume":"30","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7361-8715","authenticated-orcid":false,"given":"Jin Sug","family":"Kim","sequence":"first","affiliation":[{"name":"Department of Nephrology Juntendo University Faculty of Medicine  Tokyo Japan"},{"name":"Division of Nephrology, Department of Internal Medicine, Kyung Hee University College of Medicine Kyung Hee University Medical Center  Seoul 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Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2818-5081","authenticated-orcid":false,"given":"Maiko","family":"Nakayama","sequence":"additional","affiliation":[{"name":"Department of Nephrology Juntendo University Faculty of Medicine  Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0345-0192","authenticated-orcid":false,"given":"Yoshihito","family":"Nihei","sequence":"additional","affiliation":[{"name":"Department of Nephrology Juntendo University Faculty of Medicine  Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yusuke","family":"Suzuki","sequence":"additional","affiliation":[{"name":"Department of Nephrology Juntendo University Faculty of Medicine  Tokyo 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