Anti-mitochondrial autoantibodies in systemic lupus erythematosus and their association with disease manifestations View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-12

AUTHORS

Yann Becker, Renée-Claude Loignon, Anne-Sophie Julien, Geneviève Marcoux, Isabelle Allaeys, Tania Lévesque, Emmanuelle Rollet-Labelle, Hadrien Benk-Fortin, Nathalie Cloutier, Imène Melki, Lihi Eder, Éric Wagner, Martin Pelletier, Hassan El Hajj, Marie-Ève Tremblay, Clémence Belleannée, Marie-Josée Hébert, Mélanie Dieudé, Joyce Rauch, Paul R. Fortin, Eric Boilard

ABSTRACT

Mitochondria are organelles that govern energy supply and control cell death. Mitochondria also express bacterial features, such as the presence of inner membrane cardiolipin and a circular genome rich in hypomethylated CpG motifs. While mitochondrial extrusion by damaged organs or activated cells is thought to trigger innate immunity, it is unclear whether extracellular mitochondria also stimulate an adaptive immune response. We describe the development of novel assays to detect autoantibodies specific to two distinct components of the mitochondrion: the mitochondrial outer membrane and mitochondrial DNA. Antibodies to these two mitochondrial constituents were increased in both human and murine systemic lupus erythematosus (SLE), compared to controls, and were present at higher levels than in patients with antiphospholipid syndrome or primary biliary cirrhosis. In both bi- and multi-variate regression models, antibodies to mitochondrial DNA, but not whole mitochondria, were associated with increased anti-dsDNA antibodies and lupus nephritis. This study describes new and optimized methods for the assessment of anti-mitochondrial antibodies, and demonstrates their presence in both human and murine SLE. These findings suggest that different mitochondrial components are immunogenic in SLE, and support the concept that extracellular mitochondria may provide an important source of circulating autoantigens in SLE. More... »

PAGES

4530

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41598-019-40900-3

    DOI

    http://dx.doi.org/10.1038/s41598-019-40900-3

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1112766937

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30872710


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