02929nas a2200421 4500000000100000008004100001260001300042653002400055653002500079653001800104653001400122653002000136653001900156653001000175653001100185653001300196653001200209653002500221653002500246653002800271653002600299653001900325653000900344100001600353700001600369700001300385700001500398700001600413700001500429700001600444700001300460700001400473245011700487300001200604490000700616520187000623022001402493 1995 d c1995 May10aAntigens, Bacterial10aCD4 Lymphocyte Count10aCD4-CD8 Ratio10aCytokines10aGene Expression10aHIV Infections10aHIV-110aHumans10aLepromin10aleprosy10aLeprosy, lepromatous10aLeprosy, Tuberculoid10aLeukocytes, Mononuclear10aLymphocyte Activation10aRNA, Messenger10aSkin1 aSampaio E P1 aCaneshi J R1 aNery J A1 aDuppre N C1 aPereira G M1 aVieira L M1 aMoreira A L1 aKaplan G1 aSarno E N00aCellular immune response to Mycobacterium leprae infection in human immunodeficiency virus-infected individuals. a1848-540 v633 a
The immune responses to Mycobacterium leprae and other mycobacterial antigens were studied in 11 leprosy patients with concurrent human immunodeficiency virus type 1 (HIV-1) infection. Three patients manifested borderline lepromatous leprosy, and eight patients had borderline tuberculoid (BT) leprosy. Despite the low CD4+ T-cell count in the peripheral blood, no histologic or phenotypic change in the cellular infiltrate in either the lepromatous or tuberculoid lesions was observed when compared with HIV-1-negative patients. Lepromatous lesions contained heavily parasitized macrophages and few CD8+ T cells. Lesions from the patients with BT leprosy showed extensive CD4+ T-cell infiltration despite a significant reduction in CD4+ T-cell counts in the peripheral blood. No acid-fast bacilli were detected in the tuberculoid lesions. HIV-1 infection did not alter the lack of response in lepromatous leprosy to M. leprae antigens either in vitro or in vivo. In contrast, the skin test response to M. leprae antigens as well as the in vitro lymphoproliferative responses to mycobacterial antigens that are usually seen in patients with tuberculoid leprosy were abrogated in the BT HIV-1+ patients. However, production of gamma interferon in response to the same stimuli was preserved in most of the patients. Analysis of cytokine gene expression showed activation of additional cytokine genes in the unstimulated peripheral blood cells of patients with both leprosy and HIV-1 infections as compared with cells from patients with leprosy alone. These results suggest that granuloma formation in leprosy can be independent of the impaired CD4+ T-cell response of the HIV-1 infection. Furthermore, in HIV-1+ individuals with M. leprae infection, activation of cytokine genes is observed even when the circulating CD4+ T-cell count is significantly reduced.
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