Background: IgA1-producing cells of IgA nephropathy patients secrete IgA1 with galactose-deficientO-glycans; these IgA1 molecules form nephritogenic immune complexes. Results: Cytokines IL-6 and IL-4 accentuate IgA1 galactose deficiency via modulation of key glycosyltransferases. Conclusion: Some cytokines alter IgA1 O-glycosylation and increase production of nephritogenic IgA1 glycoforms. Significance: These data provide a mechanism explaining increased immune-complex formation in IgA nephropathy patients. © 2014 by The American Society for Biochemistry and Molecular Biology, Inc.
