CELLULAR IMMUNE-RESPONSE TO MYCOBACTERIUM-LEPRAE INFECTION IN HUMAN IMMUNODEFICIENCY VIRUS-INFECTED INDIVIDUALS

Citation
Ep. Sampaio et al., CELLULAR IMMUNE-RESPONSE TO MYCOBACTERIUM-LEPRAE INFECTION IN HUMAN IMMUNODEFICIENCY VIRUS-INFECTED INDIVIDUALS, Infection and immunity, 63(5), 1995, pp. 1848-1854
Citations number
22
Categorie Soggetti
Immunology,"Infectious Diseases
Journal title
ISSN journal
00199567
Volume
63
Issue
5
Year of publication
1995
Pages
1848 - 1854
Database
ISI
SICI code
0019-9567(1995)63:5<1848:CITMII>2.0.ZU;2-W
Abstract
The immune responses to Mycobacterium leprae and other mycobacterial a ntigens were studied in 11 leprosy patients with concurrent human immu nodeficiency virus type 1 (HIV-1) infection. Three patients manifested borderline lepromatous leprosy, and eight patients had borderline tub erculoid (BT) leprosy, Despite the low CD4(+) T-cell count in the peri pheral blood, no histologic or phenotypic change in the cellular infil trate in either the lepromatous or tuberculoid lesions was observed wh en compared with HIV-1-negative patients. Lepromatous lesions containe d heavily parasitized macrophages and Few CD8(+) T cells, Lesions from the patients with BT leprosy showed extensive CD4(+) T-cell infiltrat ion despite a significant reduction in CD4(+) T-cell counts in the per ipheral blood. No acid-fast bacilli were detected in the tuberculoid l esions. HIV-1 infection did not alter the lack of response in lepromat ous leprosy to M, leprae antigens either in vitro or in vivo, In contr ast, the skin test response to M. leprae antigens as well as the in vi tro lymphoproliferative responses to mycobacterial antigens that are u sually seen in patients with tuberculoid leprosy were abrogated in the BT HIV-1(+) patients. However, production of gamma interferon in resp onse to the same stimuli was preserved in most of the patients. Analys is of cytokine gene expression showed activation of additional cytokin e genes in the unstimulated peripheral blood cells of patients with bo th leprosy and HIV-1 infections as compared with cells from patients w ith leprosy alone. These results suggest that granuloma formation in l eprosy can be independent of the impaired CD4(+) T-cell response of th e HIV-1 infection. Furthermore, in HIV-1(+) individuals with M. leprae infection, activation of cytokine genes is observed even when the cir culating CD4(+) T-cell count is significantly reduced.