02280nas a2200385 4500000000100000008004100001260001300042653001200055653002900067653002400096653003200120653002300152653001900175653002000194653001100214653002100225653001200246653002800258653001600286653002600302653001600328653000900344653002500353653001800378653002500396653001800421100001400439700001400453700001400467245017700481300001100658490000700669520120400676022001401880 1989 d c1989 Apr10aAnimals10aAntigen-Presenting Cells10aAntigens, Bacterial10aBlood Bactericidal Activity10aCell Communication10aConcanavalin A10aHLA-DR Antigens10aHumans10aInterferon-gamma10aleprosy10aLeukocytes, Mononuclear10aLymphokines10aMacrophage Activation10aMacrophages10aMice10aMycobacterium leprae10aReceptors, Fc10aSuperoxide Dismutase10aT-Lymphocytes1 aDesai S D1 aBirdi T J1 aAntia N H00aCorrelation between macrophage activation and bactericidal function and Mycobacterium leprae antigen presentation in macrophages of leprosy patients and normal individuals. a1311-70 v573 a

The killing of Mycobacterium leprae by resting and gamma interferon (IFN-gamma)-activated macrophages in normal subjects and leprosy patients was assessed. Resting macrophages from normal individuals demonstrated the ability to kill M. leprae. For macrophages from tuberculoid patients, killing of M. leprae was only achieved in the presence of IFN-gamma, suggesting that initial T-cell activation occurs prior to the killing of M. leprae. In contrast, though activation with IFN-gamma rendered the lepromatous macrophages microbicidal, it failed to induce lymphocyte proliferation, suggesting a defect at either the antigen-presenting cell or the lymphocyte level or both. The concept that T-cell anergy is primarily due to lack of lymphokine generation was ruled out by our results, since responsiveness was restored in only a small proportion of lepromatous patients after exogenous lymphokine addition. In conclusion, this study demonstrated that killing and antigen presentation are two independent events. It appears that the ability of the macrophages per se to kill M. leprae may be of greater importance than lymphocyte-mediated activation for protection against M. leprae infection.

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