BRAIN IL-6 AND AUTISM

被引:112
作者
Wei, H. [1 ]
Alberts, I. [2 ]
Li, X. [3 ]
机构
[1] Shanxi Med Univ, Cent Lab, Shanxi Prov Peoples Hosp, Taiyuan 030012, Peoples R China
[2] CUNY, Dept Nat Sci, LaGuardia CC, New York, NY 11101 USA
[3] New York State Inst Basic Res Dev Disabil, Dept Neurochem, Staten Isl, NY 10314 USA
基金
中国国家自然科学基金;
关键词
autism; brain; Interleukin-6; neuroimmune response; behavior; CEREBELLAR GRANULE NEURONS; DENDRITIC SPINE DENSITY; INTERLEUKIN-6; IL-6; IMMUNE ACTIVATION; GENE-EXPRESSION; CHILDREN; DIFFERENTIATION; INFECTION; ELEVATION; ALTERS;
D O I
10.1016/j.neuroscience.2013.08.025
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Autism is a severe neurodevelopmental disorder characterized by impairments in social interaction, deficits in verbal and non-verbal communication, and repetitive behavior and restricted interests. Emerging evidence suggests that aberrant neuroimmune responses may contribute to phenotypic deficits and could be appropriate targets for pharmacologic intervention. Interleukin (IL)-6, one of the most important neuroimmune factors, has been shown to be involved in physiological brain development and in several neurological disorders. For instance, findings from postmortem and animal studies suggest that brain IL-6 is an important mediator of autism-like behaviors. In this review, a possible pathological mechanism behind autism is proposed, which suggests that IL-6 elevation in the brain, caused by the activated glia and/or maternal immune activation, could be an important inflammatory cytokine response involved in the mediation of autism-like behaviors through impairments of neuroanatomical structures and neuronal plasticity. Further studies to investigate whether IL-6 could be used for therapeutic interventions in autism would be of great significance. (C) 2013 IBRO. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:320 / 325
页数:6
相关论文
共 82 条
[1]   Advances in autism genetics: on the threshold of a new neurobiology [J].
Abrahams, Brett S. ;
Geschwind, Daniel H. .
NATURE REVIEWS GENETICS, 2008, 9 (05) :341-355
[2]   Linkage, association, and gene-expression analyses identify CNTNAP2 as an autism-susceptibility gene [J].
Alarcon, Maricela ;
Abrahams, Brett S. ;
Stone, Jennifer L. ;
Duvall, Jacqueline A. ;
Perederiy, Julia V. ;
Bomar, Jamee M. ;
Sebat, Jonathan ;
Wigler, Michael ;
Martin, Christa L. ;
Ledbetter, David H. ;
Nelson, Stanley E. ;
Cantor, Rita M. ;
Geschwind, Daniel H. .
AMERICAN JOURNAL OF HUMAN GENETICS, 2008, 82 (01) :150-159
[3]   A common genetic variant in the neurexin superfamily member CNTNAP2 increases familial risk of autism [J].
Arking, Dan E. ;
Cutler, David J. ;
Brune, Camille W. ;
Teslovich, Tanya M. ;
West, Kristen ;
Ikeda, Morna ;
Rea, Alexis ;
Guy, Moltu ;
Lin, Shin ;
Cook, Edwin H., Jr. ;
Chakravarti, Aravinda .
AMERICAN JOURNAL OF HUMAN GENETICS, 2008, 82 (01) :160-164
[4]   Spontaneous mucosal lymphocyte cytokine profiles in children with autism and gastrointestinal symptoms: Mucosal immune activation and reduced counter regulatory interleukin-10 [J].
Ashwood, P ;
Anthony, A ;
Torrente, F ;
Wakefield, AJ .
JOURNAL OF CLINICAL IMMUNOLOGY, 2004, 24 (06) :664-673
[5]   Altered T cell responses in children with autism [J].
Ashwood, Paul ;
Krakowiak, Paula ;
Hertz-Picciotto, Irva ;
Hansen, Robin ;
Pessah, Isaac N. ;
Van de Water, Judy .
BRAIN BEHAVIOR AND IMMUNITY, 2011, 25 (05) :840-849
[6]   Elevated plasma cytokines in autism spectrum disorders provide evidence of immune dysfunction and are associated with impaired behavioral outcome [J].
Ashwood, Paul ;
Krakowiak, Paula ;
Hertz-Picciotto, Irva ;
Hansen, Robin ;
Pessah, Isaac ;
Van de Water, Judy .
BRAIN BEHAVIOR AND IMMUNITY, 2011, 25 (01) :40-45
[7]   Molecular cytogenetic analysis and resequencing of Contactin Associated Protein-Like 2 in autism spectrum disorders [J].
Bakkaloglu, Betul ;
O'Roak, Brian J. ;
Louvi, Angeliki ;
Gupta, Abha R. ;
Abelson, Jesse E. ;
Morgan, Thomas M. ;
Chawarska, Katarzyna ;
Klin, Ami ;
Ercan-Sencicek, A. Gulhan ;
Stillman, Althea A. ;
Tanriover, Gamze ;
Abrahams, Brett S. ;
Duvall, Jackie A. ;
Robbins, Elissa M. ;
Geschwind, Daniel H. ;
Biederer, Thomas ;
Gunel, Murat ;
Lifton, Richard P. ;
State, Matthew W. .
AMERICAN JOURNAL OF HUMAN GENETICS, 2008, 82 (01) :165-173
[8]   HISTOANATOMIC OBSERVATIONS OF THE BRAIN IN EARLY INFANTILE-AUTISM [J].
BAUMAN, M ;
KEMPER, TL .
NEUROLOGY, 1985, 35 (06) :866-874
[9]   Cytokine actions in the central nervous system [J].
Benveniste, EN .
CYTOKINE & GROWTH FACTOR REVIEWS, 1998, 9 (3-4) :259-275
[10]   Multiple Events Lead to Dendritic Spine Loss in Triple Transgenic Alzheimer's Disease Mice [J].
Bittner, Tobias ;
Fuhrmann, Martin ;
Burgold, Steffen ;
Ochs, Simon M. ;
Hoffmann, Nadine ;
Mitteregger, Gerda ;
Kretzschmar, Hans ;
LaFerla, Frank M. ;
Herms, Jochen .
PLOS ONE, 2010, 5 (11)