English

Aa Ejaz,B Dass,O Kuchmak,R Mohandas

doi:10.13172/2053-0781-1-2-1092

Abstract

English

Highlights

Introduction ImmunoglobulinG4-related diseases encompass a growing list of organ involvement including membranous nephropathy, a disease entity generally associated with circulating antibodies to glomerular antigens and localised activation of complements
The latest twist is the association of IgG4 with membranous nephropathy (IgG-membr anous nephropathy (MN))[6,7], a disease entity that is generally associated with circulating antibodies to glomerular antigens and local complement activation by subepithelial immune deposit. circumstantial evidences suggest that IgG4 could have a pathogenetic role in MN, the inability of IgG4 to activate complement raises questions about the relevance of IgG4 in the pathogenesis of MN
Hypothesis We hypothesise that IgG4 molecules undergo structural perturbations via the dynamic Fab arm exchange phenomenon, which renders it capable of complement activation and a direct role in the pathogenesis of IgG4-related MN

Summary

Introduction

G4-related diseases encompass a growing list of organ involvement including membranous nephropathy, a disease entity generally associated with circulating antibodies to glomerular antigens and localised activation of complements. Both immunoglobulin G4 and complements were present in the renal biopsy specimens, the mechanistic association link between them remains uncertain, because immunoglobulin G4 is known to inhibit complement activation. Hypothesis In this article, we hypothesise that immunoglobulin G4 molecules undergo structural perturbations via the dynamic Fab arm exchange phenomenon, which might render it capable of complement activation and have a direct role in the pathogenesis of immunoglobulin G4-related membranous nephropathy. The latest twist is the association of IgG4 with membranous nephropathy (IgG-MN)[6,7], a disease entity that is generally associated with circulating antibodies to glomerular antigens and local complement activation by subepithelial immune deposit. circumstantial evidences suggest that IgG4 could have a pathogenetic role in MN, the inability of IgG4 to activate complement raises questions about the relevance of IgG4 in the pathogenesis of MN.

Results

Discussion

Conclusion