ArticleBMC infectious diseases2018
IL-17 and IL-22 production in HIV+ individuals with latent and active tuberculosis.
Article in BMC infectious diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 22 citations in OpenAlex.
- A novel diagnostic model for HIV-HTN comorbidity: genomic discovery, clinical validation, and mechanistic elucidation.Frontiers in medicine · 2026Article
- HIV impairs and exploits pulmonary Th17 and Th22 cell-mediated immune responses to Mycobacterium tuberculosis.PLoS pathogens · 2026Article
- Evaluation of Immunogenicity ofVaccines · 2025Article
- T Cell Responses during Human Immunodeficiency Virus/Vaccines · 2024Review
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- Characterization of natural killer cells in the blood and airways of cynomolgus macaques during Mycobacterium tuberculosis infection.Journal of medical primatology · 2023Article
- Current Knowledge of Th22 Cell and IL-22 Functions in Infectious Diseases.Pathogens (Basel, Switzerland) · 2023Review
- Plasma IL-33 levels and immune activation in HIV-TB coinfection: a cross-sectional study in Yaoundé, Cameroon.The Pan African medical journal · 2023Article
- Metabolites enhance innate resistance to human Mycobacterium tuberculosis infection.JCI insight · 2022Article
- Interleukin-17-A multifaceted cytokine in viral infections.Journal of cellular physiology · 2021Review
- Reduced thyroxine production in young household contacts of tuberculosis patients increases active tuberculosis disease risk.JCI insight · 2021Article
- Th22 response induced by Mycobacterium tuberculosis strains is closely related to severity of pulmonary lesions and bacillary load in patients with multi-drug-resistant tuberculosis.Clinical and experimental immunology · 2021Review
- Pulmonary MTBVAC vaccination induces immune signatures previously correlated with prevention of tuberculosis infection.Cell reports. Medicine · 2021Article
- An Integrative Network Approach to Identify Common Genes for the Therapeutics in Tuberculosis and Its Overlapping Non-Communicable Diseases.Frontiers in pharmacology · 2021Article
- Activation-Induced Marker Expression IdentifiesImmunoHorizons · 2020Article
- Article
- Small Animal Model of Post-chemotherapy Tuberculosis Relapse in the Setting of HIV Co-infection.Frontiers in cellular and infection microbiology · 2020Article
- Efferocytosis of Apoptotic Neutrophils Enhances Control of Mycobacterium tuberculosis in HIV-Coinfected Macrophages in a Myeloperoxidase-Dependent Manner.Journal of innate immunity · 2020Article
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8 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundIL-17 and IL-22 cytokines play an important role in protective immune responses against Mycobacterium tuberculosis (Mtb) infection. Information on the production of these cytokines and the factors that regulate their production in the context of human immunodeficiency virus (HIV) and latent tuberculosis infection (LTBI) or active tuberculosis disease (ATB) is limited. In the current study, we compared the production of these two cytokines by PBMC of HIV-LTBI+ and HIV + LTBI+ individuals in response to Mtb antigens CFP-10 (culture filtrate protein) and ESAT-6 (Early Secretory Antigenic Target). We also determined the mechanisms involved in their production.
methodsWe cultured Peripheral Blood Mononuclear Cells (PBMCs) from HIV- individuals and HIV+ patients with latent tuberculosis and active disease with CFP-10 and ESAT-6. Production of IL-17, IL-22 and PD1 (Programmed Death 1), ICOS (Inducible T-cell Costimulator), IL-23R and FoxP3 (Forkhead box P3) expression on CD4+ T cells was measured.
resultsIn response to Mtb antigens CFP-10 and ESAT-6, freshly isolated PBMCs from HIV+ LTBI+ and HIV+ active TB patients produced less IL-17 and IL-22 and more IL-10, expressed less IL-23R, and more PD1 and expanded to more FoxP3+ cells. Active TB infection in HIV+ individuals further inhibited antigen specific IL-17 and IL-22 production compared to those with LTBI. Neutralization of PD1 restored IL-23R expression, IL-17 and IL-22 levels and lowered IL-10 production and reduced expansion of FoxP3 T cells.
conclusionsIn the current study we found that increased PD1 expression in HIV + LTBI+ and HIV+ active TB patients inhibits IL-17, IL-22 production and IL-23R expression in response to Mtb antigens CFP-10 and ESAT-6.
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