ReviewImmunology2021
Targeting immunometabolism in host defence against Mycobacterium tuberculosis.
Review in Immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- Carbohydrates Metabolic Signatures in Immune Cells: Response to Infection.Frontiers in immunology · 2022Pooled it
- Mycobacterium tuberculosis MEM39 (Rv1977) hijacks host aldolase A (ALDOA) to subvert immunometabolism to facilitate bacterial intracellular survival.Cellular & molecular immunology · 2026Article
- Mycobacterium tuberculosis IDH-PPARγ interaction suppresses GPX4 to drive macrophage ferroptosis and sustain persistent infection.Nature communications · 2026Article
- The immunometabolic topography of cellular organization and bacterial control in tuberculosis granulomas.Nature immunology · 2026Article
- Review
- Endoplasmic Reticulum Stress in Tuberculosis: Molecular Bases and Pathophysiological Implications in the Immunopathogenesis of the Disease.International journal of molecular sciences · 2025Review
- How macrophage heterogeneity affects tuberculosis disease and therapy.Nature reviews. Immunology · 2025Review
- Glucose Metabolic Reprogramming of Macrophages AgainstImmunoTargets and therapy · 2025Review
- Where lung cancer and tuberculosis intersect: recent advances.Frontiers in immunology · 2025Review
- The diagnostic value of hydroxyproline combined with tuberculosis infection T lymphocyte spot assay in pulmonary tuberculosis.Journal of thoracic disease · 2024Article
- Article
- Tuberculous pleural effusion-induced Arg-1Respiratory research · 2024Article
- Metabolic changes enhance necroptosis of type 2 diabetes mellitus mice infected with Mycobacterium tuberculosis.PLoS pathogens · 2024Article
- Macrophages, Metabolism, Mitochondria, Circadian Rhythmicity and the Pathogen: The Multidimensional Nature of Tuberculosis.Results and problems in cell differentiation · 2024Review
- The multivalency game ruling the biology of immunity.Biophysics reviews · 2023Review
- TRAF6 triggers Mycobacterium-infected host autophagy through Rab7 ubiquitination.Cell death discovery · 2023Article
- Coevolution ofMicrobiology spectrum · 2023Article
- Immunometabolic Signature during Respiratory Viral Infection: A Potential Target for Host-Directed Therapies.Viruses · 2023Review
- Metabolic flux reprogramming inFrontiers in microbiology · 2023Article
- Antimicrobial peptides as drugs with double response againstFrontiers in microbiology · 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
2 authors at 2 institutions in 2 countries.
Funding
Abstract
In the face of ineffective vaccines, increasing antibiotic resistance and the decline in new antibacterial drugs in the pipeline, tuberculosis (TB) still remains pandemic. Exposure to Mycobacterium tuberculosis (Mtb), which causes TB, results in either direct elimination of the pathogen, most likely by the innate immune system, or infection and containment that requires both innate and adaptive immunity to form the granuloma. Host defence strategies against infectious diseases are comprised of both host resistance, which is the ability of the host to prevent invasion or to eliminate the pathogen, and disease tolerance, which is defined by limiting the collateral tissue damage. In this review, we aim to examine the metabolic demands of the immune cells involved in both host resistance and disease tolerance, chiefly the macrophage and T-lymphocyte. We will further discuss how baseline metabolic heterogeneity and inflammation-driven metabolic reprogramming during infection are linked to their key immune functions containing mycobacterial growth and instructing protective immunity. Targeting key players in immune cellular metabolism may provide a novel opportunity for treatments at different stages of TB 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.