Linked Life Data

10514092

Source:http://linkedlifedata.com/resource/pubmed/id/10514092

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pubmed-article:10514092pubmed:abstractTextMyasthenia gravis (MG) is an autoimmune disease targeting the skeletal muscle acetylcholine receptor. We have previously demonstrated a selection bias of CD4+ T cells expressing the Vbeta5.1 T-cell receptor gene in the thymus of HLA-DR3 patients with MG. To evaluate the pathogenicity of these cells, severe combined immunodeficiency mice engrafted with MG thymic lymphocytes were treated with anti-Vbeta5.1 antibody. Signs of pathogenicity (eg, acetylcholine receptor loss and complement deposits at the muscle end plates of chimeric mice) were prevented in anti-Vbeta5.1-treated severe combined immunodeficiency chimeras. Pathogenicity was mediated by autoantibodies against acetylcholine receptor. Thymic cells depleted of Vbeta5.1-positive cells in vitro before cell transfer were nonpathogenic, indicating that Vbeta5.1-positive cells are involved in the production of pathogenic autoantibodies. Acetylcholine receptor loss was prevented by Vbeta5.1 targeting in HLA-DR3 patients only, demonstrating specificity for HLA-DR3-peptide complexes. The action of the anti-Vbeta5.1 antibody involved both the in vivo depletion of Vbeta5.1-expressing cells and an increase in the interferon-gamma/interleukin-4 ratio, pointing to an immune deviation-based mechanism. This demonstration that a selective and specific T-helper cell population is involved in controlling pathogenic autoantibodies in MG holds promise for the treatment of MG.lld:pubmed
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pubmed-article:10514092pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:10514092pubmed:articleTitlePrevention of autoimmune attack by targeting specific T-cell receptors in a severe combined immunodeficiency mouse model of myasthenia gravis.lld:pubmed
pubmed-article:10514092pubmed:affiliationCNRS ESA 8078, Hôpital Marie Lannelongue, Le Plessis Robinson, France.lld:pubmed
pubmed-article:10514092pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:10514092pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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