ArticleThe Journal of clinical investigation1997
Susceptibility to anti-glomerular basement membrane disease and Goodpasture syndrome is linked to MHC class II genes and the emergence of T cell-mediated immunity in mice.
Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
42 citing papers in PubMed, 180 citations in OpenAlex.
- Growth Differentiation Factor 15 Ameliorates Anti-Glomerular Basement Membrane Glomerulonephritis in Mice.International journal of molecular sciences · 2020Article
- The Diagnostic and Clinical Utility of Autoantibodies in Systemic Vasculitis.Antibodies (Basel, Switzerland) · 2019Review
- Identification of HLA-DQA1 as a Susceptibility Gene for Spinal Tuberculosis by Exome Sequencing.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Antigen-Specificity in the Thymic Development and Peripheral Activity of CD4Frontiers in immunology · 2018Review
- The pathogenicity of T cell epitopes on human Goodpasture antigen and its critical amino acid motif.Journal of cellular and molecular medicine · 2017Article
- Antibodies against linear epitopes on Goodpasture autoantigen in patients with anti-neutrophil cytoplasmic antibody-associated vasculitis.Clinical rheumatology · 2017Article
- Basement membranes and autoimmune diseases.Matrix biology : journal of the International Society for Matrix Biology · 2017Review
- Optimizing the translational value of animal models of glomerulonephritis: insights from recent murine prototypes.American journal of physiology. Renal physiology · 2016Review
- Autoimmunity to the alpha 3 chain of type IV collagen in glomerulonephritis is triggered by 'autoantigen complementarity'.Journal of autoimmunity · 2015Article
- Identification of critical residues of linear B cell epitope on Goodpasture autoantigen.PloS one · 2015Article
- The role of necrotic cell death in the pathogenesis of immune mediated nephropathies.Clinical immunology (Orlando, Fla.) · 2014Review
- Update on crescentic glomerulonephritis.Seminars in immunopathology · 2014Review
- The HLA-DRB1*15:01-restricted Goodpasture's T cell epitope induces GN.Journal of the American Society of Nephrology : JASN · 2013Article
- Antibodies against linear epitopes on the Goodpasture autoantigen and kidney injury.Clinical journal of the American Society of Nephrology : CJASN · 2012Article
- Cutting edge issues in Goodpasture's disease.Clinical reviews in allergy & immunology · 2011Review
- Epidermal growth factor receptor promotes glomerular injury and renal failure in rapidly progressive crescentic glomerulonephritis.Nature medicine · 2011Article
- Strain differences and the genetic basis of experimental autoimmune anti-glomerular basement membrane glomerulonephritis.International journal of experimental pathology · 2011Review
- Alport alloantibodies but not Goodpasture autoantibodies induce murine glomerulonephritis: protection by quinary crosslinks locking cryptic α3(IV) collagen autoepitopes in vivo.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Macrophages and immunologic inflammation of the kidney.Seminars in nephrology · 2010Review
- Mannose receptor interacts with Fc receptors and is critical for the development of crescentic glomerulonephritis in mice.The Journal of clinical investigation · 2010Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We developed a new mouse model of human anti-glomerular basement membrane (GBM) disease to better characterize the genetic determinants of cell-mediated injury. While all major histocompatibility complex (MHC) haplotypes (H-2a, k, s, b, and d) immunized with alpha3 NC1 domains of type IV collagen produce anti-alpha3(IV) NC1 antibodies that cross-react with human Goodpasture [anti-GBM/anti-alpha3(IV) NC1] autoantibodies, only a few strains developed nephritis and lung hemorrhage associated with Goodpasture syndrome. Crescentic glomerulonephritis and lung hemorrhage were MHC-restricted in haplotypes H-2s, b, and d (A beta/A alpha region in H-2s) and associated with the emergence of an IL-12/Th1-like T cell phenotype. Lymphocytes or anti-alpha3(IV) NC1 antibodies from nephritogenic strains transfer disease to syngeneic recipients. However, passive transfer of isogenic alpha3(IV) NC1 antibodies into -/- T cell receptor-deficient mice failed to produce nephritis. Finally, nephritis and its associated IL-12/Th1-like T cell response attenuate in disease-susceptible mice tolerized orally to alpha3(IV) collagen before immunization. Our findings suggest collectively, as a hypothesis, that anti-GBM antibodies in mice only facilitate disease in MHC haplotypes capable of generating nephritogenic lymphocytes with special T cell repertoires.
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