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See 1 citation in 2017 by Bunjun R:

J Infect Dis. 2017 Dec 19;216(12):1550-1560. doi: 10.1093/infdis/jix529.

Effect of HIV on the Frequency and Number of Mycobacterium tuberculosis-Specific CD4+ T Cells in Blood and Airways During Latent M. tuberculosis Infection.

Author information

1
Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Cape Town, South Africa.
2
Division of Medical Virology, Department of Pathology, University of Cape Town, Cape Town, South Africa.
3
Wellcome Centre for Infectious Diseases Research in Africa, University of Cape Town, Cape Town, South Africa.
4
Division of Public Health Medicine, School of Public Health and Family Medicine, University of Cape Town, Cape Town, South Africa.
5
Division of Clinical Infectious Diseases, Research Center Borstel, Germany.
6
Division of Pulmonology, South Africa Department of Science and Technology-National Research Foundation, Cape Town, South Africa.
7
Centre of Excellence for Biomedical Tuberculosis Research, South Africa Department of Science and Technology-National Research Foundation, Cape Town, South Africa.
8
Division of Molecular Biology and Human Genetics, Faculty of Medicine and Health Sciences, Stellenbosch University, Cape Town, South Africa.
9
South African Medical Research Council Centre for Tuberculosis Research, Cape Town, South Africa.
10
Francis Crick Institute, London, United Kingdom.
11
Department of Medicine, Imperial College London, London, United Kingdom.

Abstract

Human immunodeficiency virus type 1 (HIV) infection substantially increases the risk of developing tuberculosis. There is extensive depletion of Mycobacterium tuberculosis-specific CD4+ T cells in blood during early HIV infection, but little is known about responses in the lungs at this stage. Given that mucosal organs are a principal target for HIV-mediated CD4+ T-cell destruction, we investigated M. tuberculosis-specific responses in bronchoalveolar lavage (BAL) from persons with latent M. tuberculosis infection and untreated HIV coinfection with preserved CD4+ T-cell counts. M. tuberculosis-specific CD4+ T-cell cytokine (interferon γ, tumor necrosis factor α, and interleukin 2) responses were discordant in frequency and function between BAL and blood. Responses in BAL were 15-fold lower in HIV-infected persons as compared to uninfected persons (P = .048), whereas blood responses were 2-fold lower (P = .006). However, an increase in T cells in the airways in HIV-infected persons resulted in the overall number of M. tuberculosis-specific CD4+ T cells in BAL being similar. Our study highlights the important insights gained from studying M. tuberculosis immunity at the site of disease during HIV infection.

KEYWORDS:

CD4+ T-cell responses; Human immunodeficiency virus; Mycobacterium tuberculosis; adaptive immunity; bronchoalveolar lavage; coinfection; lung

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