ArticlePloS one2017
LAG-3 potentiates the survival of Mycobacterium tuberculosis in host phagocytes by modulating mitochondrial signaling in an in-vitro granuloma model.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 28 citations in OpenAlex.
- Walking the tightrope: Balancing immune checkpoints and their inhibitors in host defence against bacterial infections.Journal of applied biomedicine · 2026Review
- Advanced immunotherapy across diseases and the role of artificial intelligence: A review.Biomolecules & biomedicine · 2026Review
- Article
- Regulatory Mechanisms of Co-Inhibitory Receptors in Tuberculosis Immunity: Implications for Therapeutic Targets.ImmunoTargets and therapy · 2025Review
- From immunology to artificial intelligence: revolutionizing latent tuberculosis infection diagnosis with machine learning.Military Medical Research · 2023Review
- Immunotherapy and biomarkers in patients with lung cancer with tuberculosis: Recent advances and future Directions.iScience · 2023Review
- Immunotherapies against human bacterial and fungal infectious diseases: A review.Frontiers in medicine · 2023Review
- The paradox of immune checkpoint inhibition re-activating tuberculosis.The European respiratory journal · 2022Review
- Immunosuppressive Mechanisms in Brucellosis in Light of Chronic Bacterial Diseases.Microorganisms · 2022Review
- Characterization of multiple soluble immune checkpoints in individuals with different Mycobacterium tuberculosis infection status and dynamic changes during anti-tuberculosis treatment.BMC infectious diseases · 2022Article
- Reinventing the human tuberculosis (TB) granuloma: Learning from the cancer field.Frontiers in immunology · 2022Review
- The immune landscape in tuberculosis reveals populations linked to disease and latency.Cell host & microbe · 2021Article
- Recent advances in immunotherapies against infectious diseases.Immunotherapy advances · 2021Review
- Pathogenesis of Human Immunodeficiency Virus-Journal of clinical medicine · 2020Review
- Friends and foes of tuberculosis: modulation of protective immunity.Journal of internal medicine · 2018Article
- In vivo inhibition of tryptophan catabolism reorganizes the tuberculoma and augments immune-mediated control ofProceedings of the National Academy of Sciences of the United States of America · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
CD4+ T-cell mediated Th1 immune responses are critical for immunity to TB. The immunomodulatory protein, lymphocyte activation gene-3 (LAG-3) decreases Th1-type immune responses in T-cells. LAG-3 expression is significantly induced in the lungs of macaques with active TB and correlates with increased bacterial burden. Overproduction of LAG-3 can greatly diminish responses and could lead to uncontrolled Mtb replication. To assess the effect of LAG-3 on the progression of Mtb infection, we developed a co-culture system wherein blood-derived macrophages are infected with Mtb and supplemented with macaque blood or lung derived CD4+ T-cells. Silencing LAG-3 signaling in macaque lung CD4+ T-cells enhanced killing of Mtb in co-cultures, accompanied by reduced mitochondrial electron transport and increased IFN-γ expression. Thus, LAG-3 may modulate adaptive immunity to Mtb infection by interfering with the mitochondrial apoptosis pathway. Better understanding this pathway could allow us to circumvent immune features that promote disease.
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.