Document Detail


The major histocompatibility complex and autism spectrum disorder.
MedLine Citation:
PMID:  22760919     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Autism spectrum disorder (ASD) is a complex disorder that appears to be caused by interactions between genetic changes and environmental insults during early development. A wide range of factors have been linked to the onset of ASD, but recently both genetic associations and environmental factors point to a central role for immune-related genes and immune responses to environmental stimuli. Specifically, many of the proteins encoded by the major histocompatibility complex (MHC) play a vital role in the formation, refinement, maintenance, and plasticity of the brain. Manipulations of levels of MHC molecules have illustrated how disrupted MHC signaling can significantly alter brain connectivity and function. Thus, an emerging hypothesis in our field is that disruptions in MHC expression in the developing brain caused by mutations and/or immune dysregulation may contribute to the altered brain connectivity and function characteristic of ASD. This review provides an overview of the structure and function of the three classes of MHC molecules in the immune system, healthy brain, and their possible involvement in ASD. © 2012 Wiley Periodicals, Inc. Develop Neurobiol, 2012.
Authors:
Leigh A Needleman; A Kimberley McAllister
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-7-3
Journal Detail:
Title:  Developmental neurobiology     Volume:  -     ISSN:  1932-846X     ISO Abbreviation:  -     Publication Date:  2012 Jul 
Date Detail:
Created Date:  2012-7-4     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101300215     Medline TA:  Dev Neurobiol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2012 Wiley Periodicals, Inc.
Affiliation:
Center for Neuroscience, UC Davis, 1544 Newton Court, Davis, CA 95618. lneedleman@fas.harvard.edu.
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