ArticleNature communications2025
CD4 T cell dysfunction is associated with bacterial recrudescence during chronic tuberculosis.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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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.
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Who cites it
29 citing papers in PubMed.
- Article
- Review
- NRF2-mediated inhibition of alveolar macrophage MHC II expression during Mycobacterium tuberculosis infection.Cell reports · 2026Article
- Immune endotypes in tuberculosis: Keys to decoding disease complexity.Journal of internal medicine · 2026Review
- Elimination of senescent cells with senolytic drugs as adjunctive host-directed therapy reduces tuberculosis progression in mice.Nature communications · 2026Article
- HowVaccines · 2026Review
- Enhanced tuberculosis control via leveraging dendritic cell-mediated Th1 responses in preventive and immunotherapeutic vaccine strategies.Journal of advanced research · 2026Article
- Time Course Characterization of Protective Immune Responses Following BCG Vaccination in BALB/c Mice.Pathogens (Basel, Switzerland) · 2026Article
- A CD40-OX40 co-stimulatory circuit orchestrates protective CD4Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Divergent Evolution of Tuberculosis Lesions During Treatment: A Longitudinal CT-Based Analysis of Progression and Regression Patterns.Diagnostics (Basel, Switzerland) · 2026Article
- T cell receptor clonotypes predict human leukocyte antigen allele carriage and antigen exposure history.Communications biology · 2026Article
- Species-specific iNOS expression distinguishes epithelial and myeloid IFNγ responses in tuberculosis.bioRxiv : the preprint server for biology · 2026Article
- Immune Dysregulation in HIV-TB Co-Infection: Role of Cytokines and T Cell Biomarkers-A Narrative Review.Pathogens (Basel, Switzerland) · 2026Review
- KLRG1Frontiers in cellular and infection microbiology · 2026Article
- Immunotherapy for tuberculosis: current landscape, mechanistic insights, and translational perspectives.Frontiers in immunology · 2026Review
- Immune imbalance markers: key factors in early recognition of multidrug-resistant bacterial infections in non-immunocompromised VAP patients.Frontiers in immunology · 2026Article
- Host-directed therapeutics against antimicrobial-resistant bacterial infections: emerging roles of multi-omics and systems biology.Frontiers in pharmacology · 2026Review
- Molecular signaling in coinfection: howFrontiers in immunology · 2026Review
- Secondary infections following tuberculosis: epidemiology, pathogenesis and clinical implications.Breathe (Sheffield, England) · 2026Review
- Profound immune suppression and exhaustion characterize refractory mycoplasma pneumoniae pneumonia in children.Frontiers in immunology · 2026Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
While most people contain Mycobacterium tuberculosis infection, some individuals develop active disease, usually within two years of infection. Why immunity fails after initially controlling infection is unknown. C57BL/6 mice control Mycobacterium tuberculosis for up to a year but ultimately succumb to disease. We hypothesize that the development of CD4 T cell dysfunction permits bacterial recrudescence. We developed a reductionist model to assess antigen-specific T cells during chronic infection and found evidence of CD4 T cell senescence and exhaustion. In C57BL/6 mice, CD4 T cells upregulate coinhibitory receptors and lose effector cytokine production. Single cell RNAseq shows that only a small number of CD4 T cells in the lungs of chronically infected mice are polyfunctional. While the origin and causal relationship between T-cell dysfunction and recrudescence remains uncertain, we propose T cell dysfunction leads to a feed-forward loop that causes increased bacillary numbers, greater T cell dysfunction, and progressive disease.
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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.