01916nas a2200385   4500000000100000008004100001260001600042653001500058653001000073653000900083653001100092653001100103653002200114653002100136653001200157653002600169653001600195653000900211653001600220653001400236653002500250653002500275653001700300100001300317700001500330700001300345700001600358700001400374700001300388245015500401300001000556490000800566520094200574022001401516       1986                            d  c1986 Aug 0110aAdolescent10aAdult10aAged10aFemale10aHumans10aHydrogen Peroxide10aInterferon-gamma10aleprosy10aMacrophage Activation10aMacrophages10aMale10aMiddle Aged10aMonocytes10aMycobacterium leprae10aRecombinant Proteins10aTime Factors1 aKaplan G1 aNathan C F1 aGandhi R1 aHorwitz M A1 aLevis W R1 aCohn Z A00aEffect of recombinant interferon-gamma on hydrogen peroxide-releasing capacity of monocyte-derived macrophages from patients with lepromatous leprosy.  a983-70 v1373 a<p>Monocyte-derived macrophages from 14 patients with lepromatous leprosy respond to rIFN-gamma with an enhanced secretion of H2O2 in a fashion similar to that of cells obtained from normal donors. The activation is not dependent on the cutaneous bacterial index, the length of treatment, or the stage and activity of the disease. H2O2 release can be triggered in these cells both by phorbol myristate acetate and by intact irradiated Mycobacterium leprae. Uptake of M. leprae by both normal donors' and patients' macrophages is proportional to the number of bacilli added. Prior ingestion of M. leprae does not interfere with the ability of macrophages to respond to IFN-gamma by the production of oxygen intermediates. We conclude that the immune defect in lepromatous leprosy probably results from a lack of response to M. leprae by the patients' T cells rather than an inability of mononuclear phagocytes to respond to IFN-gamma.</p>  a0022-1767