Abstract
Autism spectrum disorders (ASD) are a group of heterogeneous neurological disorders that are highly variable and are clinically characterized by deficits in social interactions, communication, and stereotypical behaviors. Prevalence has risen from 1 in 10,000 in 1972 to 1 in 59 children in the United States in 2014. This rise in prevalence could be due in part to better diagnoses and awareness, however, these together cannot solely account for such a significant rise. While causative connections have not been proven in the majority of cases, many current studies focus on the combined effects of genetics and environment. Strikingly, a distinct picture of immune dysfunction has emerged and been supported by many independent studies over the past decade. Many players in the immune-ASD puzzle may be mechanistically contributing to pathogenesis of these disorders, including skewed cytokine responses, differences in total numbers and frequencies of immune cells and their subsets, neuroinflammation, and adaptive and innate immune dysfunction, as well as altered levels of immunoglobulin and the presence of autoantibodies which have been found in a substantial number of individuals with ASD. This review summarizes the latest research linking ASD, autoimmunity and immune dysfunction, and discusses evidence of a potential autoimmune component of ASD.
Highlights
First defined as a distinct syndrome in 1943 by child psychiatrist Kanner (1943), autism spectrum disorders (ASD) are a group of heterogeneous neurological disorders that are clinically characterized by deficits in social interactions, communication, and stereotypical behaviors (Baio et al, 2018)
As many autoimmune conditions do not manifest until adulthood, the young age of most study populations is a limitation to finding associations between ASD and autoimmunity
This study looked at supplementation of folinic acid, as folate receptor autoantibodies (FRA) may be interfering with folate transport across the blood-brain barrier, and found improvement in communication, language, attention and stereotypic behaviors in treated children compared with non-supplemented ASD controls (Frye et al, 2013)
Summary
First defined as a distinct syndrome in 1943 by child psychiatrist Kanner (1943), autism spectrum disorders (ASD) are a group of heterogeneous neurological disorders that are clinically characterized by deficits in social interactions, communication, and stereotypical behaviors (Baio et al, 2018). In addition to an increased prevalence of familial and maternal autoimmunity in ASD, a subset of mothers of children with ASD (10–12%) have been found to harbor autoantibodies with reactivity to fetal brain components (summarized in Table 2), and these antibodies induce ASD-like pathology in animal models (Martin et al, 2008; Braunschweig et al, 2012b; Bauman et al, 2013). Multiple studies have since confirmed the presence of maternal autoantibodies (MAbs) with paired reactivity to 37 and 73 kDA proteins exclusive to mothers of children with ASD (Croen et al, 2008; Nordahl et al, 2013; Rossi et al, 2013) Consistent with these studies, Piras et al found that single (or combinations of) maternal anti-brain antibodies correlated with severity of language and other behavioral impairments, and that the presence of a specific autoantibody at 62 kDa in the child correlated with the presence of autoantibodies in the mother (Piras et al, 2014). Administration of autoantibodies led to decreased numbers of mature dendritic spines in the adult cortex of mice, with STIP1 blockade being the likely culprit due to its importance in neuritogenesis, the sprouting of neurites that later develop
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