Date of Award:

5-1991

Document Type:

Thesis

Degree Name:

Master of Science (MS)

Department:

Biology

Committee Chair(s)

Reed P. Warren

Committee

Reed P. Warren

Committee

Vijendra Singh

Committee

Dennis Odell

Committee

Donald Sisson

Abstract

Research into the cause of autism continues without any clear-cut answers. However, recent studies suggest that abnormalities of the immune system are associated with this disorder and autism results from failure of the immune system to regulate itself. Proper immune regulation requires that the host have the appropriate number and percentage of each population of lymphocytes and monocytes. These populations can be distinguished from one another with monoclonal antibodies that react with unique protein structures on the cell surface designated as the "cluster of differentiation" (CD) antigens.

This investigation studied the possibility that the immune abnormalities seen in autism are due to a change in the lymphocytes or monocytes in the subjects with autism. The autistic subjects as compared to age- and sex-matched control subjects exhibited several changes in their cell populations. These included a depression of total lymphocytes, CD2+ (total T cells), CD4+ (helper T cells), and CD4+CD45RA+ (the antigen-inexperienced, suppressor inducer subset of helper T cells).

Also analyzed were the siblings of the autistic subjects. A reduced percentage of CD4+ cells was seen in the male siblings as compared to unrelated males. Analyses also compared the cells of mothers and fathers of the autistic subjects with controls of mothers and fathers of normal children. No differences were seen in any of the markers used.

Findings in the literature show an increase in memory cells and a decrease in naive cells as a function of age. The data gathered in these experiments uphold this concept and are consistent with the idea that CD45RA and CDw29 are maturational states of helper T cells.

The quantitation of different immune markers on lymphoid cells seems to have been useful in the further characterization and investigation of the immune mechanism relevant to the syndrome of autism. Differences in some of the cell types were observed and may account for some of the immune abnormalities seen in autism. These differences may be the result or the cause of the syndrome. Further investigation seems necessary before a direct pathological link can be found between the body's immunity and autism.

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