Mitochondrial carrier homolog 1 (Mtch1) antibodies in neuro-Behçet's disease

Abstract Efforts for the identification of diagnostic autoantibodies for neuro-Behcet's disease (NBD) have failed. Screening of NBD patients' sera with protein macroarray identified mitochondrial carrier homolog 1 (Mtch1), an apoptosis-related protein, as a potential autoantigen. ELISA stu...

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Bibliographic Details
Published in:Journal of neuroimmunology 2013-10, Vol.263 (1), p.139-144
Main Authors: Vural, Burçak, Şehitoğlu, Elçin, Çavuş, Filiz, Yalçınkaya, Nazlı, Haytural, Hazal, Küçükerden, Melike, Ulusoy, Canan, Uğurel, Elif, Turan, Selin, Bulut, Leyla, Türkoğlu, Recai, Shugaiv, Erkingül, Kürtüncü, Murat, Atakan, Şükrü, Güre, Ali O, Gül, Ahmet, Eraksoy, Mefkure, Akman-Demir, Gülşen, Tüzün, Erdem
Format: Article
Language:English
Subjects:
Adult
Allergy and Immunology
Animals
Anti-neuronal antibody
Antibody
Autoantibodies - biosynthesis
Autoantibodies - blood
Autoimmunity
Behcet Syndrome - diagnosis
Behcet Syndrome - etiology
Behcet Syndrome - immunology
Behçet's disease
Biomarkers - blood
Female
Humans
Male
Membrane Proteins - blood
Membrane Proteins - immunology
Mitochondrial carrier homolog 1
Mitochondrial Proteins - blood
Mitochondrial Proteins - immunology
Neuro-Behçet's disease
Neurology
Nucleosomes - immunology
Nucleosomes - metabolism
Rats
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Summary:Abstract Efforts for the identification of diagnostic autoantibodies for neuro-Behcet's disease (NBD) have failed. Screening of NBD patients' sera with protein macroarray identified mitochondrial carrier homolog 1 (Mtch1), an apoptosis-related protein, as a potential autoantigen. ELISA studies showed serum Mtch1 antibodies in 68 of 144 BD patients with or without neurological involvement and in 4 of 168 controls corresponding to a sensitivity of 47.2% and specificity of 97.6%. Mtch1 antibody positive NBD patients had more attacks, increased disability and lower serum nucleosome levels. Mtch1 antibody might be involved in pathogenic mechanisms of NBD rather than being a coincidental byproduct of autoinflammation.
ISSN:0165-5728
1872-8421
DOI:10.1016/j.jneuroim.2013.08.007