Authors
Masoud Majed, Fatemeh Khani-Habibabadi, Anjali J Panicker, Sarah Reasbeck, Christopher Orlando, Jeffrey Gluckstein, Scott S Zamvil, Lilyana Amezcua, Kevin C O'Connor
Published in
Neurology(R) neuroimmunology & neuroinflammation. Volume 13. Issue 6. Pages e200652. Epub Oct 09, 2026.
Abstract
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an inflammatory demyelinating disorder of the CNS characterized by pathogenic MOG autoantibodies. Data regarding maternal-infant transfer of MOG autoantibodies, particularly in breast milk, are limited. We aimed to characterize maternal MOG autoantibodies longitudinally and assess their presence in maternal plasma, breast milk, and infant blood, as well as their clinical relevance in the infant.
MOG-specific IgG, IgA, and IgM, including selected subclass analyses, were assessed by cell-based assays in longitudinal maternal plasma and breast milk samples, as well as infant plasma at birth. Additional assays assessed epitope specificity and isoform recognition.
Maternal plasma MOG-IgG titers were persistently elevated, with transient reduction during early pregnancy. MOG-IgG and MOG-IgA were detected in maternal plasma and breast milk. Binding patterns to MOG isoforms and epitopes were near-identical between compartments and restricted to the IgG1 and IgA1 subclasses. The infant tested positive for MOG-IgG at birth. The infant remained clinically asymptomatic through 18 months, despite autoantibody detection and ongoing breastfeeding.
Maternal MOG autoantibodies in blood and breast milk were not associated with clinical disease in the infant, suggesting no increased risk of MOGAD from maternal transmission.
PMID:
42854177
Bibliographic data and abstract were imported from PubMed on 10 Oct 2026.
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