2025
Loss of GalNAc-T14 links O-glycosylation defects to alterations in B cell homing in IgA nephropathy
Prakash S, Steers N, Li Y, Sanchez-Rodriguez E, Verbitsky M, Robbins I, Simpson J, Pathak S, Raska M, Reily C, Ng A, Liang J, DeMaria N, Katiraei A, O'Stevens K, Fischman C, Shapiro S, Kodali S, McCutchan J, Park H, Eliby D, Delsante M, Allegri L, Fiaccadori E, Bodria M, Marasa M, Raveche E, Julian B, Uhlemann A, Kiryluk K, Zhang H, D'Agati V, Sanna-Cherchi S, Novak J, Gharavi A. Loss of GalNAc-T14 links O-glycosylation defects to alterations in B cell homing in IgA nephropathy. Journal Of Clinical Investigation 2025, 135: e181164. PMID: 40153534, PMCID: PMC12077892, DOI: 10.1172/jci181164.Peer-Reviewed Original ResearchConceptsO-glycosylationAberrant O-glycosylationIgA nephropathyMucosal immunityN-acetylgalactosaminyltransferaseElevated serum IgA levelsAdoptive-transfer experimentsB-cell homingSerum IgA levelsProtein O-glycosylationIgA-producing cellsGlomerular IgA depositionImmune-complex formationPathogenesis of IgANIgA1 hinge regionIgA1-producing cellsPeripheral bloodImpaired homingKidney injuryB cellsB lymphocytesIgA levelsLoF variantsIgA depositionGalNAc-T14
2024
Heterozygous mutations in factor H aggravate pathological damage in a stable IgA deposition model induced by Lactobacillus casei cell wall extract
Li J, Dong Y, Chen F, Yang H, Chen P, Li H, Shi S, Zhou X, Zhu L, Zhang Y, Liu L, Xie X, Yu F, Jin J, Lv J, Zhang H. Heterozygous mutations in factor H aggravate pathological damage in a stable IgA deposition model induced by Lactobacillus casei cell wall extract. Frontiers In Immunology 2024, 15: 1368322. PMID: 38558821, PMCID: PMC10978756, DOI: 10.3389/fimmu.2024.1368322.Peer-Reviewed Original ResearchCell wall extractsLactobacillus casei cell wall extractBiomarkers of kidney dysfunctionComplement activationFactor H mutationSeverity of glomerular lesionsPositive rate of IgAMild kidney damageDecline of kidney functionPathogenesis of IgA nephropathyProduction of IgA.Wall extractsGlomerular IgA depositionPathogenesis of IgANWild type controlsComplement overactivationElevated IgAElevated biomarkersHeterozygous mutationsC57BL/6 miceIgA-IgGKidney dysfunctionAlternative pathwayComplement inhibitorsIgA nephropathy
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