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  • Title: Defective T cell function for inhibition of growth of Mycobacterium avium-intracellulare complex (MAC) in patients with MAC disease: restoration by cytokines.
    Author: Tsukaguchi K, Yoneda T, Okamura H, Tamaki S, Takenaka H, Okamoto Y, Narita N.
    Journal: J Infect Dis; 2000 Dec; 182(6):1664-71. PubMed ID: 11069238.
    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.
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