ArticlePLoS pathogens2011
A gamma interferon independent mechanism of CD4 T cell mediated control of M. tuberculosis infection in vivo.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers.
What it found
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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.
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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
127 citing papers in PubMed, 218 citations in OpenAlex.
- Antigen Availability Shapes T Cell Differentiation and Function during Tuberculosis.Cell host & microbe · 2017Trial
- Sorting nexin 5 deficiency impairs MHC class II antigen presentation and inflammatory responses during tuberculosis.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- NRF2-mediated inhibition of alveolar macrophage MHC II expression during Mycobacterium tuberculosis infection.Cell reports · 2026Article
- HowVaccines · 2026Review
- IFNγ blockade in Mycobacterium tuberculosis infected macaques alters the granuloma environment but not bacterial control.Nature communications · 2026Article
- Sorting nexin 5 mediates antigen presentation and immunity againstbioRxiv : the preprint server for biology · 2026Article
- Strong sustained type I IFN signaling acts cell intrinsically to impair IFNγ responses and cause tuberculosis susceptibility.bioRxiv : the preprint server for biology · 2026Article
- T cell-macrophage interactions in tuberculosis: What we've got here is failure to communicate.Journal of internal medicine · 2026Review
- Article
- IFN-γ and IL-17 elicit synergistic anti-mycobacterial responses by inhibiting coronin-1A retention.Communications biology · 2025Article
- Cytotoxic granules and effector molecules from immune cells in tuberculosis: Mechanisms of host defense and therapeutic potential.Virulence · 2025Review
- Tuberculosis susceptibility in genetically diverse mice reveals functional diversity of neutrophils.eLife · 2025Article
- Tertiary Lymphoid Structures in Tuberculosis: Persistence, Protection, and Pathology.Immunological reviews · 2025Review
- Noncanonical T cell responses are associated with protection from tuberculosis in mice and humans.The Journal of experimental medicine · 2025Article
- Antigen-specific CD4+ T cells promote monocyte recruitment and differentiation into glycolytic lung macrophages to control Mycobacterium tuberculosis.PLoS pathogens · 2025Article
- CD8α marks a Mycobacterium tuberculosis-reactive human NK cell population with high activation potential.Scientific reports · 2025Article
- Article
- MetE: a promising protective antigen for tuberculosis vaccine development.Frontiers in immunology · 2025Article
- Reappraising the Role of T Cell-Derived IFN-γ in Restriction of Mycobacterium tuberculosis in the Murine Lung.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Specific CD4Nature immunology · 2024Article
67 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
CD4 T cell deficiency or defective IFNγ signaling render humans and mice highly susceptible to Mycobacterium tuberculosis (Mtb) infection. The prevailing model is that Th1 CD4 T cells produce IFNγ to activate bactericidal effector mechanisms of infected macrophages. Here we test this model by directly interrogating the effector functions of Th1 CD4 T cells required to control Mtb in vivo. While Th1 CD4 T cells specific for the Mtb antigen ESAT-6 restrict in vivo Mtb growth, this inhibition is independent of IFNγ or TNF and does not require the perforin or FAS effector pathways. Adoptive transfer of Th17 CD4 T cells specific for ESAT-6 partially inhibited Mtb growth while Th2 CD4 T cells were largely ineffective. These results imply a previously unrecognized IFNγ/TNF independent pathway that efficiently controls Mtb and suggest that optimization of this alternative effector function may provide new therapeutic avenues to combat Mtb through vaccination.
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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.