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dc.contributor.authorReynolds, Johnen_GB
dc.date.accessioned2012-06-13T11:33:37Z
dc.date.available2012-06-13T11:33:37Z
dc.date.issued2011-06
dc.identifier.citationReynolds, J. (V) 'Strain differences and the genetic basis of experimental autoimmune anti-glomerular basement membrane glomerulonephritis' International journal of experimental pathology, 92 (3):211-217 Int J Exp Patholen_GB
dc.identifier.issn1365-2613
dc.identifier.pmid21342299
dc.identifier.doi10.1111/j.1365-2613.2011.00763.x
dc.identifier.urihttp://hdl.handle.net/10547/228739
dc.description.abstractGoodpasture'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.
dc.language.isoenen
dc.publisherBlackwell Publishingen_GB
dc.relation.urlhttps://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2613.2011.00763.xen_GB
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3101493/
dc.subject.meshAnimals
dc.subject.meshAnti-Glomerular Basement Membrane Disease
dc.subject.meshDisease Models, Animal
dc.subject.meshGenetic Predisposition to Disease
dc.subject.meshImmunity, Cellular
dc.subject.meshImmunity, Humoral
dc.subject.meshMice
dc.subject.meshMice, Inbred AKR
dc.subject.meshMice, Inbred C57BL
dc.subject.meshMice, Inbred CBA
dc.subject.meshMice, Inbred DBA
dc.subject.meshRats
dc.subject.meshRats, Inbred BN
dc.subject.meshRats, Inbred F344
dc.subject.meshRats, Inbred Lew
dc.subject.meshRats, Inbred WKY
dc.titleStrain differences and the genetic basis of experimental autoimmune anti-glomerular basement membrane glomerulonephritis.en
dc.typeArticleen
dc.contributor.departmentUniversity of Bedfordshireen_GB
dc.identifier.journalInternational journal of experimental pathologyen_GB
html.description.abstractGoodpasture'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.


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