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Strain differences and the genetic basis of experimental autoimmune anti‐glomerular basement membrane glomerulonephritis
Author(s) -
Reynolds John
Publication year - 2011
Publication title -
international journal of experimental pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.671
H-Index - 72
eISSN - 1365-2613
pISSN - 0959-9673
DOI - 10.1111/j.1365-2613.2011.00763.x
Subject(s) - glomerulonephritis , autoimmunity , immunology , glomerular basement membrane , autoimmune disease , rapidly progressive glomerulonephritis , disease , pathogenesis , basement membrane , biology , medicine , immune system , pathology , kidney , genetics , antibody
Summary Goodpasture’s, or anti‐glomerular basement membrane (GBM), disease presents with rapidly progressive glomerulonephritis, caused by autoimmunity to a component of the GBM, the non‐collagenous domain of the α3 chain of type IV collagen [α3(IV)NC1]. To investigate the mechanisms of inflammation in glomerulonephritis and to test new approaches to treatment, animal models of glomerulonephritis, termed experimental autoimmune glomerulonephritis (EAG), have been developed in susceptible strains of rats and mice. This review article describes how these models of EAG have been developed over the past three decades, discusses the evidence for the involvement of both humoral and cell‐mediated immunity in the induction and pathogenesis of glomerulonephritis in these models and highlights recent, emerging data that have identified potential candidate genes that may control the genetic susceptibility in these different strains of rats and mice. The identification of these susceptibility genes has lead to a better understanding of the genetic basis of this model of anti‐GBM disease, which may be relevant to the immunopathogenesis of Goodpasture’s disease, and more generally to the progression from autoimmunity to target‐organ damage.