02045nas a2200313   4500000000100000008004100001260001300042653002400055653001100079653002300090653002400113653001800137653001800155653001200173653002600185653002500211653001800236100001700254700001600271700001200287700001500299700001400314700001200328245010900340300001000449490000700459520125100466022001401717       1984                            d  c1984 Aug10aAntigens, Bacterial10aHumans10aImmunity, Cellular10aIn Vitro Techniques10aInterleukin-110aInterleukin-210aleprosy10aLymphocyte Activation10aMycobacterium leprae10aT-Lymphocytes1 aHaregewoin A1 aMustafa A S1 aHelle I1 aWaters M F1 aLeiker DL1 aGodal T00aReversal by interleukin-2 of the T cell unresponsiveness of lepromatous leprosy to Mycobacterium leprae.  a77-860 v803 a<p>In some subjects Mycobacterium leprae causes disseminated (lepromatous) disease. Such subjects show both in vivo and in vitro deficient T cell responses to M. leprae, but not to other antigens. We have recently shown that lepromatous peripheral blood mononuclear cells (PBMC) failed to produce interleukin 2 (IL-2) in response to M. leprae and that T cell-conditioned media (TCM) can reverse the T cell unresponsiveness in a majority of lepromatous leprosy patients (Haregewoin et al. 1983). Here we show that highly purified and recombinant IL-2 had effects similar to TCM. On the other hand, lepromatous PBMC produced IL-1, and IL-1 had no restorative effect. These findings provide further evidence that the unresponsiveness in lepromatous leprosy often results from a deficiency in IL-2 production. After initial stimulation with TCM + M. leprae, lepromatous PBMC could be restimulated with M. leprae alone, providing clear evidence that M. leprae-reactive lymphocytes were generated in the presence of TCM. The present findings are discussed in relation to the possible mechanisms involved in the failure of IL-2 production. If our findings can be reproduced in vivo, IL-2 may offer a novel approach to therapy in lepromatous leprosy.</p>  a0105-2896