The Etiology of Autism and NICHD Research- Immune Findings in Autism
The following is part of the slide presentation given by Marie Bristol-Power, PhD, who serves as the Special Assistant for Autism, in the Office of the Director at the NICHD, at the March 8, 2001, meeting of the Institute of Medicine (IOM) Immunization Safety Review Committee.
Immune findings in autism
From Warren, et al. (See abstract below)
- C4B "null allele"-25/50 subjects vs. 17/85 controls
- Extended HLA haplotype B44-S30-DR4-14/50 subjects vs. 2/85 controls
- HVR-3 sequence 1-17/50 subjects vs. 2/85 controls
Abstract for Warren et. al.
Autism results from several different etiologies or combination of pathological mechanisms. Mounting evidence indicates that immune dysfunction along with an environmental pathogen may be factors contributing to the development of some cases of autism. One of the immune deficiencies observed in autism is abnormal T-cell mediated immunity. Another is altered levels of certain classes of antibodies (immunoglobulins), including 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 to be associated with autism. In the developing child, genetically determined immune deficiencies might increase the risk for autism in 2 ways: (1) A pathogen or its toxins might damage the brain, and (2) the pathogen might trigger an autoimmune mechanism that would interfere with brain functioning. In the mother, immune deficiency might allow a pathogen to persist in utero, damaging the fetal brain directly or triggering a maternal immune response that creates pathogenesis in the fetal brain. (c) 2000 APA/PsycINFO, all rights reserved.
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