Absence of glomerular IgA1 deposition despite overexpression of galactose-deficient IgA1 in the B cell c1galt1 knockout mouse - PubMed
3 hours ago
- #glycosylation
- #IgA nephropathy
- #mucosal immunity
- Study genetically disrupted the galactosyltransferase 1 gene (c1galt1) in B cells of mice expressing human IgA1, resulting in high levels of galactose-deficient IgA1 (Gd-IgA1) in circulation.
- Despite elevated Gd-IgA1, the knockout mice showed limited glomerular IgA deposition, even under inflammatory stimulation, and had impaired B cell development and reduced IgA production.
- In a passive model, IgA1 from mucosal sources in IgA nephropathy patients induced stronger mesangial deposition than serum- or myeloma-derived IgA1, despite similar or lower Gd-IgA1 content.
- Findings suggest Gd-IgA1 correlates with mucosal immune activation but is not a direct driver of kidney deposition; tissue origin and immune context are key factors in pathogenic potential.