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    Autoimmunity to the alpha 3 chain of type IV collagen in glomerulonephritis is triggered by 'autoantigen complementarity'

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    Authors
    Reynolds, John
    Preston, Gloria A.
    Pressler, Barrak M.
    Hewins, Peter
    Brown, Michael
    Roth, Aleeza
    Alderman, Elizabeth
    Bunch, Donna
    Jennette, J. Charles
    Cook, H. Terence
    Falk, Ronald J.
    Pusey, Charles D.
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    Affiliation
    Imperial College London
    University of North Carolina at Chapel Hill
    University of Bedfordshire
    Issue Date
    2015-04-02
    Subjects
    immunology
    
    Metadata
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    Abstract
    'Autoantigen complementarity' is a theory proposing that the initiator of an autoimmune response is not necessarily the autoantigen or its molecular mimic, but may instead be a peptide that is 'antisense/complementary' to the autoantigen. We investigated whether such complementary proteins play a role in the immunopathogenesis of autoimmune glomerulonephritis. Experimental autoimmune glomerulonephritis, a model of anti-glomerular basement membrane (GBM) disease, can be induced in Wistar Kyoto (WKY) rats by immunization with the α3 chain of type IV collagen. In this study, WKY rats were immunized with a complementary α3 peptide (c-α3-Gly) comprised of amino acids that 'complement' the well characterized epitope on α3(IV)NC1, pCol(24-38). Within 8 weeks post-immunization, these animals developed cresentic glomerulonephritis, similar to pCol(24-38)-immunized rats, while animals immunized with scrambled peptide were normal. Anti-idiotypic antibodies to epitopes from c-α3-Gly-immunized animals were shown to be specific for α3 protein, binding in a region containing sense pCol(24-38) sequence. Interestingly, anti-complementary α3 antibodies were identified in sera from patients with anti-GBM disease, suggesting a role for 'autoantigen complementarity' in immunopathogenesis of the human disease. This work supports the idea that autoimmune glomerulonephritis can be initiated through an immune response against a peptide that is anti-sense or complementary to the autoantigen. The implications of this discovery may be far reaching, and other autoimmune diseases could be due to responses to these once unsuspected 'complementary' antigens.
    Citation
    Reynolds J, Preston GA, Pressler BM, Hewins P, Brown M, Roth A, Alderman E, Bunch D, Jennette JC, Cook HT, Falk RJ, Pusey CD (2015) 'Autoimmunity to the alpha 3 chain of type IV collagen in glomerulonephritis is triggered by 'autoantigen complementarity'', Journal of Autoimmunity, 59 (), pp.8-18.
    Publisher
    Elsevier
    Journal
    Journal of Autoimmunity
    URI
    http://hdl.handle.net/10547/623159
    DOI
    10.1016/j.jaut.2015.01.003
    PubMed ID
    25841937
    PubMed Central ID
    PMC4459745
    Additional Links
    https://www.sciencedirect.com/science/article/pii/S0896841115000049
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4459745/
    Type
    Article
    Language
    en
    ISSN
    0896-8411
    EISSN
    0896-8411
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.jaut.2015.01.003
    Scopus Count
    Collections
    Biomedical and biological science

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