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Enzyme-linked Immunospot Assay (ELISPOT): Quantification of Th-1 Cellular Immune Responses Against Microbial Antigens
Published on: November 24, 2010
Cellular immune response to Mycobacterium leprae infection in human immunodeficiency virus-infected individuals
E P Sampaio1, J R Caneshi, J A Nery
1Leprosy Department, Oswaldo Cruz Foundation, Manguinhos, Rio de Janeiro, Brazil.
Insights
Human immunodeficiency virus type 1 (HIV-1) infection did not alter leprosy lesions, but abrogated immune responses to Mycobacterium leprae antigens in HIV-1+ patients. Cytokine gene activation occurred despite reduced CD4+ T-cell counts.
Area of Science:
- Immunology
- Infectious Diseases
- Dermatology
Background:
- Leprosy, caused by Mycobacterium leprae, presents diverse clinical forms.
- Human immunodeficiency virus type 1 (HIV-1) co-infection complicates immune responses.
- Understanding immune dynamics in co-infected individuals is crucial for treatment.
Purpose of the Study:
- To investigate immune responses to Mycobacterium leprae in leprosy patients with concurrent HIV-1 infection.
- To compare cellular infiltrates and antigen-specific responses in HIV-1+ leprosy patients versus HIV-1-negative controls.
- To analyze cytokine gene expression in co-infected individuals.
Main Methods:
- Studied 11 leprosy patients with HIV-1 co-infection (3 borderline lepromatous, 8 borderline tuberculoid).
- Assessed histologic and phenotypic changes in skin lesions.
- Evaluated in vitro and in vivo responses to Mycobacterium leprae antigens and measured gamma interferon production.
- Analyzed cytokine gene expression in peripheral blood cells.
Main Results:
- No significant histologic or phenotypic changes in lesions compared to HIV-1-negative patients.
- Lepromatous lesions showed parasitized macrophages and few CD8+ T cells.
- Borderline tuberculoid lesions had CD4+ T-cell infiltration despite reduced peripheral CD4+ counts.
- HIV-1 did not affect responses in lepromatous leprosy but abrogated skin test and lymphoproliferative responses in borderline tuberculoid HIV-1+ patients.
- Gamma interferon production was preserved.
- Increased cytokine gene activation in unstimulated peripheral blood cells of co-infected patients.
Conclusions:
- Granuloma formation in leprosy may be independent of HIV-1-impaired CD4+ T-cell response.
- HIV-1 infection in leprosy patients leads to cytokine gene activation even with significantly reduced CD4+ T-cell counts.
- Immune responses to Mycobacterium leprae are differentially affected by HIV-1 in various leprosy forms.
Abstract:
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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