02015nas a2200421 4500000000100000008004100001260001300042653001500055653001000070653000900080653002200089653002000111653001000131653003000141653001100171653002400182653001100206653002800217653002600245653001600271653000900287653001600296653002500312653003100337653002900368100002000397700001100417700001400428700001500442700001300457700001600470700001600486245012700502300000900629490000700638520093400645022001401579 1995 d c1995 Jan10aAdolescent10aAdult10aAged10aAged, 80 and over10aCells, Cultured10aChild10aCytotoxicity, Immunologic10aFemale10aHeat-Shock Proteins10aHumans10aLeukocytes, Mononuclear10aLymphocyte Activation10aMacrophages10aMale10aMiddle Aged10aMycobacterium leprae10aMycobacterium tuberculosis10aT-Lymphocytes, Cytotoxic1 aDe La Barrera S1 aFink S1 aFiniasz M1 aMinnucci F1 aValdez R1 aBaliƱa L M1 aSasiain M C00aLack of cytotoxic activity against Mycobacterium leprae 65-kD heat shock protein (hsp) in multibacillary leprosy patients. a90-70 v993 a

Cytotoxic T cells play an important role in host defence mechanisms, as well as in the immunopathology of leprosy. In this study, we evaluated whether Mycobacterium leprae hsp18, hsp65 and Myco. tuberculosis hsp71 could induce cytotoxic T cell activity against autologous macrophages pulsed with these hsp. Paucibacillary (PB) patients and normal controls generated more effector cells than multibacillary (MB) patients with all three hsp tested. There was no cross-reactivity between any of the hsp tested. Mycobacterium leprae hsp65 induced cytotoxic responses only in those MB patients undergoing an erythema nodosum leprosum (ENL) episode. Although hsp65 and hsp18 induced similar proliferation in MB patients, a high proportion of these patients did not generate cytotoxic effector cells in response to hsp65. Hence, those T cells reacting to hsp65 may play an important role in the control of Myco. leprae infection.

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