ArticleJournal of immunology (Baltimore, Md. : 1950)2023
High Bacillary Burden and the ESX-1 Type VII Secretion System Promote MHC Class I Presentation by Mycobacterium tuberculosis-Infected Macrophages to CD8 T Cells.
Article in Journal of immunology (Baltimore, Md. : 1950), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 18 citations in OpenAlex.
- Host-pathogen interactions in tuberculosis: from immunological mechanisms to translational applications.Cell insight · 2026Review
- Human memory CD4bioRxiv : the preprint server for biology · 2026Article
- HowVaccines · 2026Review
- Improved immune responses and tuberculosis protection by aerosol vaccination with recombinant BCG expressing ESX-1 from Mycobacterium marinum.PLoS pathogens · 2026Article
- CD8+ lymphocytes in immunity against tuberculosis.Journal of immunology (Baltimore, Md. : 1950) · 2026Review
- NR4A1 limits CD8Research square · 2026Article
- NR4A1 limits CD8⁺ T Cell effector responses and protection in tuberculosis.bioRxiv : the preprint server for biology · 2026Article
- Functional analysis of type VII secretion system links to host immune evasion mechanism inFrontiers in cellular and infection microbiology · 2026Review
- T cell-macrophage interactions in tuberculosis: What we've got here is failure to communicate.Journal of internal medicine · 2026Review
- Mycobacterium tuberculosis biology, pathogenicity and interaction with the host.Nature reviews. Microbiology · 2025Review
- Control of antigen presentation on MHC-I by a bacterial secretion system.bioRxiv : the preprint server for biology · 2025Article
- Finding and filling the knowledge gaps in mechanisms of T cell-mediated TB immunity to inform vaccine design.Nature reviews. Immunology · 2025Review
- CD226 identifies effector CD8Cell reports · 2025Article
- Tuberculosis vaccines and therapeutic drug: challenges and future directions.Molecular biomedicine · 2025Review
- Heterogeneity in lung macrophage control of Mycobacterium tuberculosis is modulated by T cells.Nature communications · 2024Article
- From pathogenesis to antigens: the key to shaping the future of TB vaccines.Frontiers in immunology · 2024Review
- Heterogeneity in lung macrophage control ofbioRxiv : the preprint server for biology · 2023Article
- Key advances in vaccine development for tuberculosis-success and challenges.NPJ vaccines · 2023Review
- Recognition and control ofFrontiers in tuberculosis · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
We used a mouse model to study how Mycobacterium tuberculosis subverts host defenses to persist in macrophages despite immune pressure. CD4 T cells can recognize macrophages infected with a single bacillus in vitro. Under identical conditions, CD8 T cells inefficiently recognize infected macrophages and fail to restrict M. tuberculosis growth, although they can inhibit M. tuberculosis growth during high-burden intracellular infection. We show that high intracellular M. tuberculosis numbers cause macrophage death, leading other macrophages to scavenge cellular debris and cross-present the TB10.4 Ag to CD8 T cells. Presentation by infected macrophages requires M. tuberculosis to have a functional ESX-1 type VII secretion system. These data indicate that phagosomal membrane damage and cell death promote MHC class I presentation of the immunodominant Ag TB10.4 by macrophages. Although this mode of Ag presentation stimulates cytokine production that we presume would be host beneficial, killing of uninfected cells could worsen immunopathology. We suggest that shifting the focus of CD8 T cell recognition to uninfected macrophages would limit the interaction of CD8 T cells with infected macrophages and impair CD8 T cell-mediated resolution of tuberculosis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.