[Immunological aspects of Mycobacterium avium complex infection]

Tuberculin anergy is common in patients with Mycobacterium avium complex (MAC) infection. We examined in vitro cell-mediated immunity in these patients with MAC infection. Peripheral blood lymphocytes of patients, as compared with those of tuberculous patients or tuberculin-positive healthy donors, showed depressed in vitro blastogenic responses to purified protein derivative of tuberculin (PPD), not only to PPDs of Mycobacterium tuberculosis but also to PPD-B and PPD-Y of M. intracellulare and M. kansasii, respectively. Analysis of defective in vitro PPD-induced lymphocyte blastogenic responses in these patients revealed that PPD-induced interleukin 2 (IL-2) production was impaired whereas PPD-induced IL-2 responsiveness was normally developed after PPD stimulation. In the second half of this report, study was carried out to examine the mechanism of depressed T cell activity in these patients. Heat-killed MAC organisms and their lipid component impaired the capacity of peripheral blood lymphocytes to proliferate in vitro in response to concanavalin A (Con A), PPD, and to a lesser degree, phytohemagglutinin (PHA) stimulation. Inhibition by MAC was not contingent upon prior exposure of the donor to MAC or other mycobacteria and occurred with lymphocytes from tuberculin-negative as well as -positive subjects. The suppression was not due to the toxicity of MAC. Adherent cell depletion and cell mixing experiments with T cells indicated that monocytes and not T cells were a major contributor to the immunosuppression observed. Treatment of monocytes with MAC or MAC-derived lipid resulted in significant decreases in CD11b, a member of the LFA-1 and Leu M3 (CD14) molecule.(ABSTRACT TRUNCATED AT 250 WORDS)