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Study of Circulating Antibodies to Heat-Shock Proteins 60 and 70 in Autistic Subjects

Autism is a behavioral syndrome characterized by a severe impairment of reciprocal social relations, and of verbal and nonverbal communications. Many different etiologic factors such as viral infection and genetic predisposition have been proposed to explain the development of this disorder. Immune abnormalities, such as a decreased lymphoblastic response to T-cell mitogen, defective antibody responses to rubella vaccine, and decreased numbers of T lymphocytes, also have been identified in a subpopulation of patients with autism, which implies that the development of autism in some cases may be due to autoimmune mechanisms.
Recent evidence suggests that immune response to the heat-shock proteins 60 and 70 is associated with several autoimmune diseases, including juvenile arthritis, type 1 diabetes, and multiple sclerosis. Therefore, in this study, the plasmas of patients with autism were examined by enzyme linked immunosorbent assay (ELISA) for antibodies to the heat-shock proteins 60 and 70.
The autistic subjects were found to have increased levels of antibodies against heat-shock protein 70 as compared to that of age-matched controls (p=O. 0148). However, levels of antibodies to heat shock protein 60 in the autistic subjects showed considerable individual variation and no significant difference was found.
Abnormal immune reactions to myelin basic protein have also been found in autistic subjects. Since epitopes on myelin basic protein have been shown to crossreact with determinants on heat-shock protein 60, the similarity between anti-myelin basic protein monoclonal antibodies and antiheat- shock protein 60 antibodies in the autistic subjects was also studied. The results showed no crossreactivity between these two antibodies.
In conclusion, the data from the study of antibodies against heat-shock protein 70 suggest an elevated immune response to heat-shock protein 70 in autistic subjects. This result implies that autism could be an autoimmune disease.

Identiferoai:union.ndltd.org:UTAHS/oai:digitalcommons.usu.edu:etd-5688
Date01 May 1994
CreatorsChiu, Fang-Yi
PublisherDigitalCommons@USU
Source SetsUtah State University
Detected LanguageEnglish
Typetext
Formatapplication/pdf
SourceAll Graduate Theses and Dissertations
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