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- W2766652804 abstract "Autism Spectrum Disorder (ASD) is a complex brain disorder and a pressing medical concern, affecting over 1% of children in the United States. ASD is considered a neurodevelopmental disorder, resulting from problems during neural development that lead to neural circuit dysfunction and abnormal behavior in the postnatal life. Increasing evidence supports an important role of the immune system in the pathogenesis of ASD. Moreover, changes in immune function play important roles in brain development and behavior. Although immune dysfunction during development has been implicated in ASD, the underlying mechanisms are poorly understood. The endoplasmic reticulum (ER) is a major site of protein synthesis. Many of the ASD risk factors during pregnancy as well as genetic variations in several synaptic genes implicated in ASD have been shown to induce ER stress. It is known that prolonged ER stress leads to the production of many proinflammatory molecules. Our study found that maternal ER stress induced by the nucleoside antibiotic tunicamycin at embryonic day 12.5 (E12.5) in mice increases IL-17a signaling and ASD-like behaviors in the offspring. Anti-IL-17a antibody treatment blocks maternal ER stress-induced ASD-like behavior in the offspring. Given the important role of immune function in ASD, identifying novel regulatory mechanisms may provide avenues to develop newer therapeutics." @default.
- W2766652804 created "2017-11-10" @default.
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- W2766652804 date "2017-11-01" @default.
- W2766652804 modified "2023-09-26" @default.
- W2766652804 title "Maternal ER stress induces ASD-like behavior in mice through the IL-17a pathway" @default.
- W2766652804 doi "https://doi.org/10.1016/j.bbi.2017.07.090" @default.
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