ArticleJournal of immunology (Baltimore, Md. : 1950)2008
Central tolerance regulates B cells reactive with Goodpasture antigen alpha3(IV)NC1 collagen.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- A murine Ig light chain transgene reveals IGKV3 gene contributions to anti-collagen types IV and II specificities.Molecular immunology · 2017Article
- Humanized Immunoglobulin Mice: Models for HIV Vaccine Testing and Studying the Broadly Neutralizing Antibody Problem.Advances in immunology · 2017Review
- Basement membranes and autoimmune diseases.Matrix biology : journal of the International Society for Matrix Biology · 2017Review
- Uncommon structural motifs dominate the antigen binding site in human autoantibodies reactive with basement membrane collagen.Molecular immunology · 2016Article
- Targeting Anti-Insulin B Cell Receptors Improves Receptor Editing in Type 1 Diabetes-Prone Mice.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Recovery of a human natural antibody against the noncollagenous-1 domain of type IV collagen using humanized models.Journal of translational medicine · 2015Article
- The HLA-DRB1*15:01-restricted Goodpasture's T cell epitope induces GN.Journal of the American Society of Nephrology : JASN · 2013Article
- Genetic elimination of α3(IV) collagen fails to rescue anti-collagen B cells.Immunology letters · 2011Article
- B cell receptor editing in tolerance and autoimmunity.Annals of the New York Academy of Sciences · 2011Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Patients and rodents with Goodpasture's syndrome (GPS) develop severe autoimmune crescentic glomerulonephritis, kidney failure, and lung hemorrhage due to binding of pathogenic autoantibodies to the NC1 domain of the alpha3 chain of type IV collagen. Target epitopes are cryptic, normally hidden from circulating Abs by protein-protein interactions and the highly tissue-restricted expression of the alpha3(IV) collagen chain. Based on this limited Ag exposure, it has been suggested that target epitopes are not available as B cell tolerogens. To determine how pathogenic anti-GPS autoantibody responses are regulated, we generated an Ig transgenic (Tg) mouse model that expresses an Ig that binds alpha3(IV)NC1 collagen epitopes recognized by serum IgG of patients with GPS. Phenotypic analysis reveals B cell depletion and L chain editing in Tg mice. To determine the default tolerance phenotype in the absence of receptor editing and endogenous lymphocyte populations, we crossed Tg mice two generations with mice deficient in Rag. Resulting Tg Rag-deficient mice have central B cell deletion. Thus, development of Tg anti-alpha3(IV)NC1 collagen B cells is halted in the bone marrow, at which point the cells are deleted unless rescued by a Rag enzyme-dependent process, such as editing. The central tolerance phenotype implies that tolerizing self-Ag is expressed in bone marrow.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.