Publication:
Myelin oligodendrocyte glycoprotein antibodies in genetic leukodystrophies

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dc.contributor.coauthorEroğlu Ertuğrul, Nesibe Gevher
dc.contributor.coauthorPekgüzel, Faruk
dc.contributor.coauthorGuenbey, Ceren
dc.contributor.coauthorTopçu, Meral
dc.contributor.coauthorOğuz, Kader K.
dc.contributor.coauthorÖzkara, Hatice Asuman
dc.contributor.coauthorAnlar, Banu
dc.contributor.departmentKUTTAM (Koç University Research Center for Translational Medicine)
dc.contributor.departmentGraduate School of Health Sciences
dc.contributor.departmentSchool of Medicine
dc.contributor.kuauthorDoran, Tansu
dc.contributor.kuauthorVural, Atay
dc.contributor.kuauthorYousefi, Mohammadreza
dc.contributor.schoolcollegeinstituteGRADUATE SCHOOL OF HEALTH SCIENCES
dc.contributor.schoolcollegeinstituteResearch Center
dc.contributor.schoolcollegeinstituteSCHOOL OF MEDICINE
dc.date.accessioned2024-11-09T23:18:37Z
dc.date.issued2022
dc.description.abstractAccumulation of intermediate metabolites due to enzyme deficiencies and demyelination can provoke inflammation in genetic leukodystrophies. Thirty patients with genetic leukodystrophy and 48 healthy control sera were tested for anti-myelin oligodendrocyte glycoprotein (MOG) antibodies by fixed and/or live cell-based assays. MOG-IgG was detected in two late infantile metachromatic leukodystrophy (MLD) cases, both of which were also weakly positive for IgG1, and one with IgG3 as the dominant anti-MOG IgG subclass. MOG-IgG was borderline positive in a vanishing white matter (VWM) disease patient. These results suggest that inherited metabolic or degenerative processes can have an autoimmune component, possibly as an epiphenomenon.
dc.description.indexedbyWOS
dc.description.indexedbyScopus
dc.description.indexedbyPubMed
dc.description.openaccessNO
dc.description.publisherscopeInternational
dc.description.sponsoredbyTubitakEuN/A
dc.description.sponsorshipHacettepe University Scientific Research Coordination Unit [TSA-2017-12891]
dc.description.sponsorshipScientific and Technological Research Council of Turkey [118S397]
dc.description.sponsorshipKoc University Research Center for Translational Medicine (KUTTAM)- Department of Strategy and Budget, Presidency of Turkey This study was supported by the Hacettepe University Scientific Research Coordination Unit, TSA-2017-12891. The live cell-based assay used in this study was performed with a TUBITAK3501 grant from The Scientific and Technological Research Council of Turkey, grant number 118S397. The authors acknowledge the use of the services and facilities of the Koc University Research Center for Translational Medicine (KUTTAM) , funded by the Department of Strategy and Budget, Presidency of Turkey. We thank our patients and their families for their participation in the study.
dc.description.volume369
dc.identifier.doi10.1016/j.jneuroim.2022.577916
dc.identifier.eissn1872-8421
dc.identifier.issn0165-5728
dc.identifier.quartileQ3
dc.identifier.scopus2-s2.0-85132503287
dc.identifier.urihttps://doi.org/10.1016/j.jneuroim.2022.577916
dc.identifier.urihttps://hdl.handle.net/20.500.14288/10411
dc.identifier.wos819442600003
dc.keywordsLeukodystrophy
dc.keywordsMyelin oligodendrocyte glycoprotein
dc.keywordsFixed cell-based assay
dc.keywordsLive cell-based assay
dc.keywordsMOG antibody disease (MOGAD)
dc.keywordsDemyelination
dc.language.isoeng
dc.publisherElsevier
dc.relation.ispartofJournal of Neuroimmunology
dc.subjectImmunology
dc.subjectNeurosciences
dc.titleMyelin oligodendrocyte glycoprotein antibodies in genetic leukodystrophies
dc.typeJournal Article
dspace.entity.typePublication
local.contributor.kuauthorYousefi, Mohammadreza
local.contributor.kuauthorDoran, Tansu
local.contributor.kuauthorVural, Atay
local.publication.orgunit1GRADUATE SCHOOL OF HEALTH SCIENCES
local.publication.orgunit1SCHOOL OF MEDICINE
local.publication.orgunit1Research Center
local.publication.orgunit2KUTTAM (Koç University Research Center for Translational Medicine)
local.publication.orgunit2School of Medicine
local.publication.orgunit2Graduate School of Health Sciences
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