POSSIBLE IMMUNOGENETIC BASIS FOR AUTISM

Citation
Ra. Burger et Rp. Warren, POSSIBLE IMMUNOGENETIC BASIS FOR AUTISM, Mental retardation and developmental disabilities research reviews, 4(2), 1998, pp. 137-141
Citations number
27
Categorie Soggetti
Psychology,Psychiatry,"Behavioral Sciences",Neurosciences,"Clinical Neurology",Pediatrics
ISSN journal
10804013
Volume
4
Issue
2
Year of publication
1998
Pages
137 - 141
Database
ISI
SICI code
1080-4013(1998)4:2<137:PIBFA>2.0.ZU;2-E
Abstract
Autism results from several different etiologies or combination of pat hological mechanisms. Mounting evidence indicates that immune dysfunct ion along with an environmental pathogen may be factors contributing t o the development of some cases of autism. One of the immune deficienc ies observed in autism is abnormal T-cell mediated immunity. Another i s altered levels of certain classes of antibodies (immunoglobulins), i ncluding decreased levels of immunoglobulin A and deficient complement activity, based on the inheritance of a null allele of the C4B gene. In addition to the C4B gene, other genes on chromosome 6 also appear t o be associated with autism. In the developing child, genetically dete rmined immune deficiencies might increase the risk for autism in two w ays: 1) A pathogen or its toxins might damage the brain, 2) the pathog en might trigger an autoimmune mechanism that would interfere with bra in functioning. In the mother, immune deficiency might allow a pathoge n to persist in utero, damaging the feta I brain directly or triggerin g a maternal immune response that creates pathogenesis in the feta I b rain, (C) 1998 Wiley-Liss, Inc.