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

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NATURE REVIEWS NEUROSCIENCE
卷 16, 期 8, 页码 469-486

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NATURE PUBLISHING GROUP
DOI: 10.1038/nrn3978

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资金

  1. Dennis Weatherstone Predoctoral Fellowship from Autism Speaks [7825]
  2. ARCS (Achievement Rewards for College Scientists) Foundation
  3. University of California Office of the President
  4. National Institute of Neurological Disorders and Stroke (NINDS) [R01-NS060125-05]
  5. National Institute of Mental Health (NIMH) [P50-MH106438-01]
  6. Simons Foundation (SFARI) [321998]
  7. University of California Davis Research Investments in Science and Engineering Program
  8. NATIONAL INSTITUTE OF MENTAL HEALTH [P50MH106438, F32MH010643] Funding Source: NIH RePORTER
  9. NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS060125] Funding Source: NIH RePORTER

向作者/读者索取更多资源

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.

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