Immune mediators in the brain and peripheral tissues in autism spectrum disorder.

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Title: Immune mediators in the brain and peripheral tissues in autism spectrum disorder.
Authors: Estes, Myka L., McAllister, A. Kimberley
Source: Nature Reviews Neuroscience. Aug2015, Vol. 16 Issue 8, p469-486. 18p. 3 Diagrams, 1 Chart.
Subjects: Autism spectrum disorders, Brain, Cytokines, Pervasive child development disorders, Central nervous system
Abstract: Increasing evidence points to a central role for immune dysregulation in autism spectrum disorder (ASD). Several ASD risk genes encode components of the immune system and many maternal immune system-related risk factors - including autoimmunity, infection and fetal reactive antibodies - are associated with ASD. In addition, there is evidence of ongoing immune dysregulation in individuals with ASD and in animal models of this disorder. Recently, several molecular signalling pathways - including pathways downstream of cytokines, the receptor MET, major histocompatibility complex class I molecules, microglia and complement factors - have been identified that link immune activation to ASD phenotypes. Together, these findings indicate that the immune system is a point of convergence for multiple ASD-related genetic and environmental risk factors. [ABSTRACT FROM AUTHOR]
Copyright of Nature Reviews Neuroscience is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Immune mediators in the brain and peripheral tissues in autism spectrum disorder.
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  Data: <searchLink fieldCode="AR" term="%22Estes%2C+Myka+L%2E%22">Estes, Myka L.</searchLink><br /><searchLink fieldCode="AR" term="%22McAllister%2C+A%2E+Kimberley%22">McAllister, A. Kimberley</searchLink>
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  Data: <searchLink fieldCode="DE" term="%22Autism+spectrum+disorders%22">Autism spectrum disorders</searchLink><br /><searchLink fieldCode="DE" term="%22Brain%22">Brain</searchLink><br /><searchLink fieldCode="DE" term="%22Cytokines%22">Cytokines</searchLink><br /><searchLink fieldCode="DE" term="%22Pervasive+child+development+disorders%22">Pervasive child development disorders</searchLink><br /><searchLink fieldCode="DE" term="%22Central+nervous+system%22">Central nervous system</searchLink>
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  Data: Increasing evidence points to a central role for immune dysregulation in autism spectrum disorder (ASD). Several ASD risk genes encode components of the immune system and many maternal immune system-related risk factors - including autoimmunity, infection and fetal reactive antibodies - are associated with ASD. In addition, there is evidence of ongoing immune dysregulation in individuals with ASD and in animal models of this disorder. Recently, several molecular signalling pathways - including pathways downstream of cytokines, the receptor MET, major histocompatibility complex class I molecules, microglia and complement factors - have been identified that link immune activation to ASD phenotypes. Together, these findings indicate that the immune system is a point of convergence for multiple ASD-related genetic and environmental risk factors. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Nature Reviews Neuroscience is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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