Autism Studies and Related Medical Conditions, January 2009 - TACA

largely unknown, but genetic, environmental, immunological, and neurological
factors are thought to play a role in the development of ASD. Recently,
increasing research has focused on the connections between the immune system
and the nervous system, including its possible role in the development of ASD.
These neuroimmune interactions begin early during embryogenesis and persist
throughout an individual's lifetime, with successful neurodevelopment contingent
upon a normal balanced immune response. Immune aberrations consistent with
a dysregulated immune response, which so far, have been reported in autistic
children, include abnormal or skewed T helper cell type 1 (T(H)1)/T(H)2 cytokine
profiles, decreased lymphocyte numbers, decreased T cell mitogen response, and
the imbalance of serum immunoglobulin levels. In addition, autism has been
linked with autoimmunity and an association with immune-based genes including
human leukocyte antigen (HLA)-DRB1 and complement C4 alleles described.
There is potential that such aberrant immune activity during vulnerable and
critical periods of neurodevelopment could participate in the generation of
neurological dysfunction characteristic of ASD. This review will examine the
status of the research linking the immune response with ASD.
PMID: 16698940 [PubMed - indexed for MEDLINE]
Bach JF. Infections and autoimmune diseases. J Autoimmun. 2005;25 Suppl:74-80.
Laboratoire d'Immunologie, Hôpital Necker, 161 rue de Sèvres, 75743 Paris
Cedex 15, France. bach@necker.fr
The high percentage of disease-discordant pairs of monozygotic twins
demonstrates the central role of environmental factors in the etiology of
autoimmune diseases. Efforts were first focussed on the search for triggering
factors. The study of animal models has clearly shown that infections may trigger
autoimmune diseases, as in the case of Coxsackie B4 virus in type I diabetes and
the encephalomyocarditis virus in autoimmune myositis, two models in which
viruses are thought to act by increasing immunogenicity of autoantigens
secondary to local inflammation. The induction of a Guillain-Barré syndrome in
rabbits after immunization with a peptide derived from Campylobacter jejuni is
explained by mimicry between C. jejuni antigens and peripheral nerve axonal
antigens. Other models involve chemical modification of autoantigens, as in the
case of iodine-induced autoimmune thyroiditis. These mechanisms have so far
only limited clinical counterparts (rheumatic fever, Guillain-Barré syndrome and
drug-induced lupus or myasthenia gravis) but one may assume that unknown
viruses may be at the origin of a number of chronic autoimmune diseases, such
as type I diabetes and multiple sclerosis) as illustrated by the convergent data
incriminating IFN-alpha in the pathophysiology of type I diabetes and systemic
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