ArticleJournal of immunology (Baltimore, Md. : 1950)2012
CD4+ T cell-dependent IFN-γ production by CD8+ effector T cells in Mycobacterium tuberculosis infection.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 69 citations in OpenAlex.
- Immunometabolic and RAAS determinants of circulating interferon gamma in an HIV and TB Zambian cohort.Discover public health · 2026Article
- Enhancing tuberculosis vaccine efficacy with a heterologous mRNA-ChAdOx1 prime-pull strategy targeting lung-resident memory T cells.Frontiers in immunology · 2026Article
- T cell-macrophage interactions in tuberculosis: What we've got here is failure to communicate.Journal of internal medicine · 2026Review
- Histone demethylase JMJD2D promotes macrophage IL-12b expression and contributes to host defense againstFrontiers in cellular and infection microbiology · 2026Article
- Tuberculosis susceptibility in genetically diverse mice reveals functional diversity of neutrophils.eLife · 2025Article
- IFNγ Expression Correlates with Enhanced Cytotoxicity in CD8+ T Cells.International journal of molecular sciences · 2025Article
- Single-cell RNA sequencing in tuberculosis: Application and future perspectives.Chinese medical journal · 2025Review
- Pan-Variant SARS-CoV-2 Vaccines Induce Protective Immunity by Targeting Conserved Epitopes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Distinctive Immunological Signatures Define Foot-and-Mouth Disease Virus Persistence in Vaccinated Cattle.Transboundary and emerging diseases · 2025Article
- Mycobacterium tuberculosis resides in lysosome-poor monocyte-derived lung cells during chronic infection.PLoS pathogens · 2024Article
- Bystander activated CD8Nature communications · 2024Article
- Advances of Long Non-Coding RNAs as Potential Biomarkers for Tuberculosis: New Hope for Diagnosis?Pharmaceutics · 2023Review
- Potential molecular mechanisms of chronic fatigue in long haul COVID and other viral diseases.Infectious agents and cancer · 2023Review
- Use of transcutaneous electrical acupoint stimulation in pulmonary surgery for patients with tuberculosis.Journal of clinical tuberculosis and other mycobacterial diseases · 2022Article
- Single-cell immune profiling reveals functional diversity of T cells in tuberculous pleural effusion.The Journal of experimental medicine · 2022Article
- CD4 T cell help prevents CD8 T cell exhaustion and promotes control of Mycobacterium tuberculosis infection.Cell reports · 2021Article
- Evaluation of the performance of QuantiFERON®-TB Gold plus test in active tuberculosis patients.Journal of clinical tuberculosis and other mycobacterial diseases · 2021Article
- Airway delivery of both a BCG prime and adenoviral boost drives CD4 and CD8 T cells into the lung tissue parenchyma.Scientific reports · 2020Article
- Article
- Recognition of CD8The European respiratory journal · 2019Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Both CD4+ and CD8+ T cells contribute to immunity to tuberculosis, and both can produce the essential effector cytokine IFN-γ. However, the precise role and relative contribution of each cell type to in vivo IFN-γ production are incompletely understood. To identify and quantitate the cells that produce IFN-γ at the site of Mycobacterium tuberculosis infection in mice, we used direct intracellular cytokine staining ex vivo without restimulation. We found that CD4+ and CD8+ cells were predominantly responsible for production of this cytokine in vivo, and we observed a remarkable linear correlation between the fraction of CD4+ cells and the fraction of CD8+ cells producing IFN-γ in the lungs. In the absence of CD4+ cells, a reduced fraction of CD8+ cells was actively producing IFN-γ in vivo, suggesting that CD4+ effector cells are continually required for optimal IFN-γ production by CD8+ effector cells. Accordingly, when infected mice were treated i.v. with an MHC-II-restricted M. tuberculosis epitope peptide to stimulate CD4+ cells in vivo, we observed rapid activation of both CD4+ and CD8+ cells in the lungs. Indirect activation of CD8+ cells was dependent on the presence of CD4+ cells but independent of IFN-g responsiveness of the CD8+ cells. These data provide evidence that CD4+ cell deficiency impairs IFN-γ production by CD8+ effector cells and that ongoing cross-talk between distinct effector T cell types in the lungs may contribute to a protective immune response against M. tuberculosis. Conversely, defects in these interactions may contribute to susceptibility to tuberculosis and other infections.
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