01825nas a2200229   4500000000100000008004100001260001700042653002300059653001100082653003000093653002300123653001200146653001600158653001600174100001900190245005600209300001100265490000700276050003200283520126600315022001401581       1992                            d  c1992 Jul-Sep10aBacterial Vaccines10aHumans10aHypersensitivity, Delayed10aImmunity, Cellular10aleprosy10aLymphocytes10aMacrophages1 aChatterjee B R00aLeprosy immunopathogenesis and vaccine development.  a359-740 v64  aInfolep Library - available3 a<p>The truly effective immunity against intracellular parasites, including mycobacteria, is mediated by monocyte/macrophages, and in the immunologically responding (resistant) host these phagocytes need minimal antigenic stimulus, specific or non-specific, to become activated and be microbicidal. T-cell mediated delayed hypersensitivity (DTH) causes tissue damage and destruction, which is particularly unwelcome in leprosy because of its nerve-damaging potential. Gamma interferon (INF-gamma), the terminal lymphokine of a DTH response, promotes mycobacterial survival and growth. There are T-cells (TH1 subtypes) that produce DH response either independent of, or, only partly dependent on INF-gamma; this type of DH peaking at 24 hours appears similar to the Jones-Mote type rather than to the tuberculin type of DTH peaking at 48-72 hours and is devoid of the necrotic component of tuberculin type of DTH. M. leprae antigens normally elicit this Jones-Mote type of DH. Suppressor T-cells are associated with a protective immune response, while helper T-cells mediating DTH are harmful. In view of this immunobiology, it would appear that pathogenic mycobacteria that generate a tuberculin type DTH response should not be used as immunogens in leprosy.</p>  a0254-9395