Defective T cell function for inhibition of growth of Mycobacterium avium-intracellulare complex (MAC) in patients with MAC disease: restoration by cytokines.

Abstract

To define the immunopathologic mechanism underlying pulmonary Mycobacterium avium-intracellulare complex (MAC) disease in patients without AIDS, the ability of CD4(+) and gammadelta 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-gamma and macrophage colony-stimulating factor decreased in patients. CD4(+) T and gammadelta 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 gammadelta 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.