02353nas a2200385 4500000000100000008004100001260001300042653003100055653002000086653002500106653001500131653001400146653002000160653001100180653003000191653002300221653002500244653002100269653001800290653002500308653002500333653001600358653002900374653003400403653003000437100001900467700001500486700001700501700001700518245008300535300001100618490000800629520131600637022001401953 1990 d c1990 Apr10aCD4-Positive T-Lymphocytes10aDendritic Cells10aDinitrochlorobenzene10aFoam Cells10aGranuloma10aHLA-DR Antigens10aHumans10aHypersensitivity, Delayed10aImmunity, Cellular10aImmunohistochemistry10aInterferon-gamma10aKeratinocytes10aLeprosy, lepromatous10aLeprosy, Tuberculoid10aMacrophages10aReceptors, Interleukin-210aT-Lymphocytes, Helper-Inducer10aT-Lymphocytes, Regulatory1 aVolc-Platzer B1 aKremsner P1 aStemberger H1 aWiedermann G00aRestoration of defective cytokine activity within lepromatous leprosy lesions. a458-660 v2723 a

Immunohistological studies of tuberculoid leprosy lesions (TT-lesions) showed a dense, well organized granuloma consisting of a central area with epitheloid and giant cells containing interferon-gamma (IFN-Gamma) and CD3+, CD4+ T helper/inducer (Th/i) cells, a considerable proportion of which expressed the interleukin-2-receptor (IL-2 R). This central area was surrounded by round cells which consisted mainly of CD3+/CD8+ T cytotoxic/suppressor (Tc/s) lymphocytes. The overlying keratinocytes (KC) were strongly positive for HLA-DR antigens on the surface, indicating high intralesional IFN-Gamma activity. In contrast, lepromatous leprosy lesions (LL-lesions) showed a disorganized infiltrate composed by foamy cells and round cells, the latter mainly expressing the CD3+/CD8+ phenotype. IFN-Gamma activity could not be detected within the lesions. The KC overlying the infiltrate were consistently negative for HLA/DR reactivity pointing to a defective intralesional IFN-Gamma production in LL patients. Two out of four patients with LL leprosy could be sensitized with dinitrochlorobenzene (DNCB). The eliciting of DNCB skin reactions within the LL-lesion led to the recruitment of new infiltrating cells; the resulting infiltrate resembled a local reversal towards the tuberculoid pole of leprosy.

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