ArticleThe American journal of pathology2009
Mucosal tolerance induced by an immunodominant peptide from rat alpha3(IV)NC1 in established experimental autoimmune glomerulonephritis.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 16 citations in OpenAlex.
- A Modified Peptide Derived from Goodpasture Autoantigen Arrested and Attenuated Kidney Injuries in a Rat Model of Anti-GBM Glomerulonephritis.Journal of the American Society of Nephrology : JASN · 2020Article
- The role of the immune system in kidney disease.Clinical and experimental immunology · 2018Review
- Immune Response against Autoantigen PLA2R Is not Gambling: Implications for Pathophysiology, Prognosis, and Therapy.Journal of the American Society of Nephrology : JASN · 2016Article
- Myeloperoxidase Peptide-Based Nasal Tolerance in Experimental ANCA-Associated GN.Journal of the American Society of Nephrology : JASN · 2016Article
- Autoimmunity to the alpha 3 chain of type IV collagen in glomerulonephritis is triggered by 'autoantigen complementarity'.Journal of autoimmunity · 2015Article
- Spleen tyrosine kinase inhibition attenuates autoantibody production and reverses experimental autoimmune GN.Journal of the American Society of Nephrology : JASN · 2014Article
- Strain differences and the genetic basis of experimental autoimmune anti-glomerular basement membrane glomerulonephritis.International journal of experimental pathology · 2011Review
- The self/nonself issue: A confrontation between proteomes.Self/nonself · 2010Article
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Authors and funding
5 authors at 2 institutions in 1 country.
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Abstract
Experimental autoimmune glomerulonephritis (EAG), an animal model of Goodpasture's disease, can be induced in Wistar Kyoto (WKY) rats by immunization with the noncollagenous domain of the alpha 3 chain of type IV collagen, alpha3(IV)NC1. Recent studies have identified an immunodominant peptide, pCol (24-38), from the N-terminus of rat alpha3(IV)NC1; this peptide contains the major B- and T-cell epitopes in EAG and can induce crescentic nephritis. In this study, we investigated the mechanisms of mucosal tolerance in EAG by examining the effects of the nasal administration of this peptide after the onset of disease. A dose-dependent effect was observed: a dose of 300 microg had no effect, a dose of 1000 microg resulted in a moderate reduction in EAG severity, and a dose of 3000 microg produced a marked reduction in EAG severity accompanied by diminished antigen-specific, T-cell proliferative responses. These results demonstrate that mucosal tolerance in EAG can be induced by nasal administration of an immunodominant peptide from the N-terminus of alpha3(IV)NC1 and should be of value in designing new therapeutic strategies for patients with Goodpasture's disease and other autoimmune disorders.
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