Characterization of immune cell phenotypes in adults with autism spectrum disorders

Autism spectrum disorders (ASDs) are neurodevelopmental disorders characterized by impairments in verbal and non-verbal communication, impaired social interactions and repetitive behaviors. There is evidence of a link between ASD symptoms and immune dysfunction, but few studies have been performed i...

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Published inJournal of investigative medicine Vol. 64; no. 7; pp. 1179 - 1185
Main Authors López-Cacho, José Manuel, Gallardo, Soledad, Posada, Manuel, Aguerri, Miriam, Calzada, David, Mayayo, Teodoro, Lahoz, Carlos, Cárdaba, Blanca
Format Journal Article
LanguageEnglish
Published Los Angeles, CA SAGE Publications 01.10.2016
Sage Publications Ltd
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Summary:Autism spectrum disorders (ASDs) are neurodevelopmental disorders characterized by impairments in verbal and non-verbal communication, impaired social interactions and repetitive behaviors. There is evidence of a link between ASD symptoms and immune dysfunction, but few studies have been performed in adult patients to confirm this. In this work, we used flow cytometry to study immunological differences in peripheral blood mononuclear cells from 59 adult patients and 26 healthy control subjects to identify possible immune cell profiles related with this group of disorders. We analyzed six immune cell subpopulations (ie, B-cells, CD4+ and CD8+ T-cells, NK, NKT cells, and monocytes) and their corresponding stages of apoptosis and activation. The most noteworthy results showed that, compared to healthy controls, patients had increased percentages of CD8+ T-cells and B-cells, and a decrease in the percentage of NKT cells. Regarding CD25 expression, we found overall CD25+ overexpression, primarily in NK and NKT cells. Apoptosis percentage showed an increasing trend only in monocytes of patients. These data support a link between ASD and immune dysfunction, suggesting that specific cellular phenotypes and/or activation status of immune cells may be relevant in adult ASD.
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ISSN:1081-5589
1708-8267
DOI:10.1136/jim-2016-000070