Detection of MOG-IgG and MOG-IgA in Maternal Breast Milk and Infant Blood in MOGAD: A Case Report.
5 affiliations
- 1Department of Neurology, Keck School of Medicine, University of Southern California, Los Angeles.
- 2Departments of Neurology and Immunobiology, Yale School of Medicine, Yale University, New Haven, CT.
- 3Department of Ophthalmology, Keck School of Medicine, University of Southern California, Los Angeles.
- 4Department of Neurology & Weill Institute for Neurosciences, University of California, San Francisco; and.
- 5Program in Immunology, University of California, San Francisco.
Abstract
Background and objectives
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.Methods
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.Results
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.Discussion
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.
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BibTeX
@article{majed2026detection,
title = {{Detection of MOG-IgG and MOG-IgA in Maternal Breast Milk and Infant Blood in MOGAD: A Case Report.}},
author = {Masoud Majed and Fatemeh Khani-Habibabadi and Anjali J Panicker and Sarah Reasbeck and Christopher Orlando and Jeffrey Gluckstein and Scott S Zamvil and Lilyana Amezcua and Kevin C O'Connor},
journal = {Neurology(R) neuroimmunology \& neuroinflammation},
year = {2026},
month = oct,
doi = {10.1212/nxi.0000000000200652},
url = {https://europepmc.org/article/MED/42854177},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - Detection of MOG-IgG and MOG-IgA in Maternal Breast Milk and Infant Blood in MOGAD: A Case Report.
AU - Masoud Majed
AU - Fatemeh Khani-Habibabadi
AU - Anjali J Panicker
AU - Sarah Reasbeck
AU - Christopher Orlando
AU - Jeffrey Gluckstein
AU - Scott S Zamvil
AU - Lilyana Amezcua
AU - Kevin C O'Connor
PY - 2026
DA - 2026/10/09
JO - Neurology(R) neuroimmunology & neuroinflammation
DO - 10.1212/nxi.0000000000200652
UR - https://europepmc.org/article/MED/42854177
AB - Background and objectives 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.Methods 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.Results 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.Discussion 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.
SN - 2332-7812
ER -