In measles encephalitis we: Confirmed the decrease in mitogen responses and have shown that it does not correlate with complications. Demonstrated that the 'immunosuppression' is not universal but may be an abnormality of immune regulation as shown by the response to measles virus and myelin basic protein and by an abnormality of suppressor cell activity in patients with measles. Have evidence that there is early demyelination, and a response to myelin basic protein in a large proportion of the patients, and a lack of evidence of direct virus invasion of the brain. These findings lead to our present hypothesis that measles virus infection, probably of lymphoid cells, leads to a breakdown of immune regulation. This lack of regulation may lead to dissemination and allow secondary infection. It may also lead to a break in tolerance leading to autoimmune demyelination, a regulation which as Patterson (1979) has said 'may effectively restrain our ever present capacity to react immunologically against our own nervous tissue'.