01987nas a2200349   4500000000100000008004100001260001300042653002000055653002000075653001100095653002100106653001800127653001800145653001300163653001200176653001600188653003100204653002700235653002900262653000900291100001900300700001700319700001200336700002000348700001700368245009200385856009000477300001100567490000700578520103800585022001401623       1988                            d  c1988 Feb10aEpidermal Cells10aHLA-DR Antigens10aHumans10aInterferon-gamma10aInterleukin-110aInterleukin-210aKeratins10aleprosy10aMacrophages10aReceptors, Antigen, T-Cell10aReceptors, Immunologic10aReceptors, Interleukin-210aSkin1 aVolc-Platzer B1 aStemberger H1 aLuger T1 aRadaszkiewicz T1 aWiedermann G00aDefective intralesional interferon-gamma activity in patients with lepromatous leprosy.  uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1541447/pdf/clinexpimmunol00101-0031.pdf  a235-400 v713 a<p>Cryostat sections of full-thickness skin biopsies from 21 patients along the whole spectrum of leprosy were subjected to immunohistological examination with special regard to defective lymphokine production. There was an inverse relationship between intra-lesional IL-1 reactivity and IL-2R expression, in that the latter was markedly observed in tuberculoid lesions. Whenever epithelioid cell containing granulomas were present in paucibacillary forms, significant reactivity within the central phagocytic cells with the monoclonal antibody directed against interferon-gamma was detectable. The keratinocytes covering tuberculoid lesions abundantly expressed class II alloantigens (HLA-DR antigens), indicating high intra-lesional interferon-gamma activity. In contrast, multibacillary forms revealed significant anti-IL-1 reactivity within the cellular infiltrate. IL-2R bearing cells were virtually absent as was anti-HLA-DR reactivity of the keratinocytes, underlining a defective intra-lesional interferon-gamma activity.</p>  a0009-9104