We have begun an investigation on the immune systems of patients with autism in attempt to determine if immune mechanisms are involved in the development of this severe developmental disorder. A study of 31 autistic patients has revealed several immune-system abnormalities, including reduced responsiveness in the lymphocyte blastogenesis assay to phytohemagglutinin, concanavalin A, and pokeweed mitogen; decreased numbers of T lymphocytes; and an altered ratio of helper to suppressor T cells. Immune-system abnormalities may be directly related to underlying biologic processes of autism, or these changes may be an indirect reflection of the actual pathologic mechanism.

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The effects of hyperoxia on lung tumor development were examined in mice and rats. In mice, exposure to 70% O2 prevented the development of urethan- or 3-methylcholanthrene-induced lung tumors. Dietary antioxidants [butylated hydroxytoluene (BHT) and butylated hydroxyanisole (BHA)] were unable to prevent the inhibition of tumor development by oxygen, although BHT retained its capability to enhance tumor development in mouse lung. In visible-size tumors, oxygen did not depress DNA synthesis. Oxygen also reduced the number of pulmonary metastatic nodules after i.v. injection of mammary gland-derived carcinoma cells, but failed to inhibit growth of murine lung carcinoma or murine melanoma-derived cell lines. Rats treated with one single intratracheal instillation of 3-methylcholanthrene developed multiple lung lesions; their growth could be prevented by exposure of the animals to 40 or 70% O2. It is concluded that hyperoxia prevents development of transformed cells in vivo in the lung and may affect adversely the growth of selected cell lines metastatic to the lung.

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A number of immune abnormalities have been found in epileptic patients. Several, but not all, of these defects appear to be related to the toxic effects of antiseizure medications. To study the basis of immune abnormalities in epilepsy, various populations and subsets of peripheral blood mononuclear cells (PBMC) from epileptic patients were enumerated and their functions examined. Reduced natural killer cell activity was found in the patients and their siblings. Enumeration of the PBMC showed a lower proportions of Leu 11+ cells in some of the patients which may account for the lower natural killer activity. A reduced ratio of OKT4+/OKT8+ cells was also found in the patients. Responses of patient PBMC to the T-cell mitogens phytohemagglutinin, concanavalin A and the B-cell mitogen pokeweed mitogen were unchanged as were the total number of rosette-forming cells in the patients. The results provide more evidence for a genetic basis for some of the immune abnormalities in epileptic patients.