| Abstract
| - To define the immunopathologic mechanism underlying pulmonary Mycobacterium avium—intracellulare complex (MAC) disease in patients without AIDS, the ability of CD4+ and yd T cells to induce growth inhibition of MAC in monocytes was compared between patients and healthy control subjects. T cell—dependent growth inhibition and production of interferon-γ and macrophage colony—stimulating factor decreased in patients. CD4+ T and γδ T cells from patients were equally defective in inducing anti-MAC activity. The combination of these cytokines restored the ability of patients' T cells to control MAC growth. In experiments with allogeneic cocultures of γδ T cells and infected monocytes from patients and control subjects, healthy control T cells could augment growth inhibition of MAC in monocytes from patients, whereas patients' T cells could not, even in the presence of healthy control monocytes. These results indicate that the defect in T cells may be associated with impaired protective immunity against MAC in these patients.
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