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Complement activating antibodies to myelin oligodendrocyte glycoprotein in neuromyelitis optica and related disorders
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نویسنده
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mader s. ,gredler v. ,schanda k. ,rostasy k. ,dujmovic i. ,pfaller k. ,lutterotti a. ,jarius s. ,di pauli f. ,kuenz b. ,ehling r. ,hegen h. ,deisenhammer f. ,aboul-enein f. ,storch m.k. ,koson p. ,drulovic j. ,kristoferitsch w. ,berger t. ,reindl m.
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منبع
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journal of neuroinflammation - 2011 - دوره : 8 - شماره : 0
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چکیده
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Background: serum autoantibodies against the water channel aquaporin-4 (aqp4) are important diagnostic biomarkers and pathogenic factors for neuromyelitis optica (nmo). however,aqp4-igg are absent in 5-40% of all nmo patients and the target of the autoimmune response in these patients is unknown. since recent studies indicate that autoimmune responses to myelin oligodendrocyte glycoprotein (mog) can induce an nmo-like disease in experimental animal models,we speculate that mog might be an autoantigen in aqp4-igg seronegative nmo. although high-titer autoantibodies to human native mog were mainly detected in a subgroup of pediatric acute disseminated encephalomyelitis (adem) and multiple sclerosis (ms) patients,their role in nmo and high-risk nmo (hr-nmo; recurrent optic neuritis-ron or longitudinally extensive transverse myelitis-letm) remains unresolved.results: we analyzed patients with definite nmo (n = 45),hr-nmo (n = 53),adem (n = 33),clinically isolated syndromes presenting with myelitis or optic neuritis (cis,n = 32),ms (n = 71) and controls (n = 101; 24 other neurological diseases-ond,27 systemic lupus erythematosus-sle and 50 healthy subjects) for serum igg to mog and aqp4. furthermore,we investigated whether these antibodies can mediate complement dependent cytotoxicity (cdc). aqp4-igg was found in patients with nmo (n = 43,96%),hr-nmo (n = 32,60%) and in one cis patient (3%),but was absent in adem,ms and controls. high-titer mog-igg was found in patients with adem (n = 14,42%),nmo (n = 3,7%),hr-nmo (n = 7,13%,5 ron and 2 letm),cis (n = 2,6%),ms (n = 2,3%) and controls (n = 3,3%,two sle and one ond). two of the three mog-igg positive nmo patients and all seven mog-igg positive hr-nmo patients were negative for aqp4-igg. thus,mog-igg were found in both aqp4-igg seronegative nmo patients and seven of 21 (33%) aqp4-igg negative hr-nmo patients. antibodies to mog and aqp4 were predominantly of the igg1 subtype,and were able to mediate cdc at high-titer levels.conclusions: we could show for the first time that a subset of aqp4-igg seronegative patients with nmo and hr-nmo exhibit a mog-igg mediated immune response,whereas mog is not a target antigen in cases with an aqp4-directed humoral immune response. © 2011 mader et al; licensee biomed central ltd.
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کلیدواژه
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Aquaporin-4; Autoantibodies; Biomarker; Complement mediated cytotoxicity; Myelin oligodendrocyte glycoprotein; Neuromyelitis optica
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آدرس
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clinical department of neurology,innsbruck medical university,innsbruck, Austria, clinical department of neurology,innsbruck medical university,innsbruck, Austria, clinical department of neurology,innsbruck medical university,innsbruck, Austria, department of pediatrics iv,division of pediatric neurology and inborn errors of metabolism,innsbruck medical university,innsbruck, Austria, clinic of neurology,clinical center of serbia,belgrade, Serbia, division of histology and embryology,innsbruck medical university, Austria, clinical department of neurology,innsbruck medical university,innsbruck, Austria, division of molecular neuroimmunology,department of neurology,university of heidelberg,heidelberg, Germany, clinical department of neurology,innsbruck medical university,innsbruck, Austria, clinical department of neurology,innsbruck medical university,innsbruck, Austria, clinical department of neurology,innsbruck medical university,innsbruck, Austria, clinical department of neurology,innsbruck medical university,innsbruck, Austria, clinical department of neurology,innsbruck medical university,innsbruck, Austria, department of neurology,smz-ost donauspital,vienna, Austria, department of neurology,medical university of graz,graz, Austria, department of neurology,slovak medical university,university hospital ruzinov,bratislava,slovakia,institute of neuroimmunology,slovak academy of sciences,bratislava, Slovakia, clinic of neurology,clinical center of serbia,belgrade,serbia,faculty of medicine,university of belgrade,belgrade, Serbia, karl landsteiner institute for neuroimmunological and neurodegenerative disorders,vienna, Austria, clinical department of neurology,innsbruck medical university,innsbruck, Austria, clinical department of neurology,innsbruck medical university,innsbruck, Austria
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