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Review

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Role of Aberrant Glycosylation of IgA1 Molecules in the Pathogenesis of IgA Nephropathy

Mestecky J.a, b, g · Tomana M.b · Moldoveanu Z.a · Julian B.A.a, b · Suzuki H.a, f · Matousovic K.a, g · Renfrow M.B.c · Novak L.d · Wyatt R.J.e · Novak J.a

Author affiliations

Departments of aMicrobiology, bMedicine, cBiochemistry/Molecular Genetics, and dPathology, University of Alabama at Birmingham, Birmingham, Ala., and eUniversity of Tennessee Health Science Center, Memphis, Tenn., USA; fJuntendo University School of Medicine, Tokyo, Japan; gCharles University, Schools of Medicine, Prague and Pilsen, Czech Republic

Corresponding Author

Jiri Mestecky, MD, PhD

Department of Microbiology, University of Alabama at Birmingham

Box 1 845, 19th Street South

Birmingham, AL 35294-2170 (USA)

Tel. +1 205 934 2225, Fax +1 205 934 3894, E-Mail mestecky@uab.edu

Related Articles for ""

Kidney Blood Press Res 2008;31:29–37

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Abstract

Studies of the properties of immune complexes (IC) in the circulation, urine, and mesangium of IgA nephropathy (IgAN) patients have provided data relevant to the pathogenesis of this disease. IC contain predominantly polymeric IgA1 molecules which are deficient in galactose (Gal) residues on O-linked glycan chains in the hinge region (HR) of their heavy (H) chains. As a result of this aberrancy, a novel antigenic determinant(s) involving N-acetylgalactosamine (GalNAc) and perhaps sialic acid (SA) of O-linked glycans is generated and recognized by naturally occurring GalNAc-specific antibodies. Thus, IC in IgAN consist of Gal-deficient IgA1 molecules as an antigen, and GalNAc-specific IgG and/or IgA1 as an antibody. IgG antibodies to Gal-deficient IgA1 are probably induced by cross-reactive microbial antigens; they are present at variable levels not only in humans with or without IgAN but also in many phylogenetically diverse vertebrate species. Incubation of human mesangial cells with IC from sera of IgAN patients indicated that stimulation of cellular proliferative activity was restricted to the large (>800 kDa) complexes. These findings suggest that experimental approaches that prevent the formation of large Gal-deficient IgA1-IgG IC may be applied ultimately in an immunologically mediated therapy.

© 2008 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Review

Received: September 19, 2007
Accepted: November 02, 2007
Published online: January 08, 2008
Issue release date: February 2008

Number of Print Pages: 9
Number of Figures: 3
Number of Tables: 1

ISSN: 1420-4096 (Print)
eISSN: 1423-0143 (Online)

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