Journal
BRAIN BEHAVIOR & IMMUNITY-HEALTH
Volume 33, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.bbih.2023.100678
Keywords
Synapsin-I; Antineuronal autoantibodies; Transplacental transfer; Maternofetal autoimmunity; Growth retardation; Peptide microarray
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This study found that synapsin-I autoantibodies produced during pregnancy may have detrimental effects on fetal development and are closely associated with developmental abnormalities and neuropsychiatric developmental disorders.
Anti-neuronal autoantibodies can be transplacentally transferred during pregnancy and may cause detrimental effects on fetal development. It is unclear whether autoantibodies against synapsin-I, one of the most abundant synaptic proteins, are associated with developmental abnormalities in humans. We recruited a cohort of 263 pregnant women and detected serum synapsin-I IgG autoantibodies in 13.3% using cell-based assays. Seropositivity was strongly associated with abnormalities of fetal development including structural defects, intrauterine growth retardation, amniotic fluid disorders and neuropsychiatric developmental diseases in previous children (odds ratios of 3-6.5). Autoantibodies reached the fetal circulation and were mainly of IgG1/IgG3 subclasses. They bound to conformational and linear synapsin-I epitopes, five distinct epitopes were identified using peptide microarrays. The findings indicate that synapsin-I autoantibodies may be clinically useful biomarkers or even directly participate in the disease process of neurodevelopmental disorders, thus being potentially amenable to antibody-targeting interventional strategies in the future.
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