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Other studies have suggested that abnormalities in mucosal immunity and lymphocyte homing are major contributors to disease. We identified a family with IgAN segregating a heterozygous predicted loss-of-function (LOF) variant in\n                    <jats:italic>GALNT14<\/jats:italic>\n                    , the gene encoding\n                    <jats:italic>N<\/jats:italic>\n                    -acetylgalactosaminyltransferase 14, one of the enzymes involved in mucin-type protein\n                    <jats:italic>O<\/jats:italic>\n                    -glycosylation. While\n                    <jats:italic>GALNT14<\/jats:italic>\n                    is expressed in IgA1-producing cells, carriers of the LOF variant did not have altered levels of poorly glycosylated IgA1, suggesting other disease mechanisms. Investigation of\n                    <jats:italic>Galnt14<\/jats:italic>\n                    -null mice revealed elevated serum IgA levels and ex vivo IgA production by B cells. These mice developed glomerular IgA deposition with aging and after induction of sterile colitis.\n                    <jats:italic>Galnt14<\/jats:italic>\n                    -null mice also displayed an attenuated mucin layer in the colon and redistribution of IgA-producing cells from mucosal to systemic sites. Adoptive-transfer experiments indicated impaired homing of spleen-derived\n                    <jats:italic>Galnt14<\/jats:italic>\n                    -deficient B lymphocytes, resulting in increased retention in peripheral blood. These findings suggest that abnormalities in\n                    <jats:italic>O<\/jats:italic>\n                    -glycosylation alter mucosal immunity and B lymphocyte homing, pointing to an expanded role of aberrant\n                    <jats:italic>O<\/jats:italic>\n                    -glycosylation in the pathogenesis of IgAN.\n                  <\/jats:p>","DOI":"10.1172\/jci181164","type":"journal-article","created":{"date-parts":[[2025,3,28]],"date-time":"2025-03-28T14:36:09Z","timestamp":1743172569000},"source":"Crossref","is-referenced-by-count":17,"title":["Loss of GalNAc-T14 links O-glycosylation defects to alterations in B cell homing in IgA nephropathy"],"prefix":"10.1172","volume":"135","author":[{"given":"Sindhuri","family":"Prakash","sequence":"first","affiliation":[{"name":"Department of Medicine, Division of Nephrology, Columbia University Irving Medical Center, College of Physicians and Surgeons, New York, New York, 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