Abstract
Autism Spectrum Disorder (ASD) comprises a group of neurodevelopmental conditions whose etiology involves complex interactions between genetic and environmental factors. Among the latter, maternal infection during pregnancy is known to trigger Maternal Immune Activation (MIA), a process that can alter fetal neurodevelopment by releasing proinflammatory cytokines. In this context, Candida albicans, a commensal fungus of the gastrointestinal and genitourinary tracts, has been proposed as a potential inducer of MIA during gestation, when hormonal changes and maternal immunomodulation favor its proliferation. The present study evaluated serum levels of anti-C. albicans immunoglobulin G (IgG) in three groups: mothers of children with ASD, mothers of neurotypical children, and nulliparous women. Results showed lower IgG levels in mothers of neurotypical children, whereas mothers of children with ASD exhibited values comparable to those of nulliparous women. These findings suggest that reduced antifungal reactivity during pregnancy may reflect a protective immunological adaptation, while the absence of such modulation could indicate persistent inflammatory reactivity associated with ASD risk. Therefore, this study proposes that the risk of autism is not linked to maternal hyperimmunity but rather to a dysfunction in gestational immune tolerance. The immune response to C. albicans is thus proposed as a potential biomarker of maternal–fetal regulation and neurodevelopmental risk.
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