01804nas a2200265   4500000000100000008004100001260000900042653001100051653002300062653002400085653001800109653001200127653002600139653001400165653001500179653001800194653003000212100001300242700001300255245006200268300001000330490000700340520117700347022001401524       1985                            d  c198510aHumans10aImmunity, Cellular10aIn Vitro Techniques10aInterleukin-210aleprosy10aLymphocyte Activation10aMonocytes10aPhagocytes10aT-Lymphocytes10aT-Lymphocytes, Regulatory1 aKaplan G1 aCohn Z A00aCellular immunity in lepromatous and tuberculoid leprosy.  a205-90 v113 a<p>The depression of cellular immunity in lepromatous patients is not understood. While the blood monocytes of leprosy patients appear to be activated normally by lymphokines, T cell proliferation and production of lymphokines in response to Mycobacterium leprae are impaired in lepromatous patients. Attempts to restore responsiveness in cells from these patients have been unsuccessful in our hands. The addition of exogenous IL-2 to leukocyte cultures does not appear to restore responsiveness to M. leprae in cells from nonresponder patients. Rather, some enhancement, often not antigen specific, is observed in cells from patients with a preexisting response. Similarly, depletion of monocytes does not restore responsiveness to M. leprae in non-responder patients, but a nonspecific enhancement of proliferation is observed in monocyte-free cultures from patients that do respond to M. leprae. Thus, the defect in lepromatous non-responder patients does not result from a simple lack of IL-2 production or suppression by monocytes and/or their products. Possibly, there is a low level or lack of M. leprae responsive T cells in the circulation of these patients.</p>  a0165-2478