Abstract
Chronic treatment of BALB/c mice with ultraviolet (uv) radiation produces two distinct immunologic deficiencies. These deficiencies are apparent long before visible skin tumors are induced by the uv irradiation. One is reflected in a transient inability to develop delayed hypersensitivity to dinitrochlorobenzene and appears to be due to a defect in antigen processing. The other is expressed by the failure of mice to reject syngeneic uv-induced tumors, which are highly antigenic. This lack of tumor rejection can be passively transferred with lymphoid cells and seems to be due to the presence of specific suppressor lymphocytes.
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