ReviewNature reviews. Immunology2025
How macrophage heterogeneity affects tuberculosis disease and therapy.
Review in Nature reviews. Immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed.
- Strong, sustained type I IFN signaling acts cell intrinsically to impair IFNγ responses and cause tuberculosis susceptibility.Cell host & microbe · 2026Article
- Ubiquitylation by the GID/CTLH complex regulates the metabolic and innate immune response of macrophages to infection by Mycobacterium tuberculosis.PLoS pathogens · 2026Article
- In tuberculosis, the neutrophil is neutral in name alone.Nature immunology · 2026Article
- Airway immune signatures of protection and disease progression in recent human tuberculosis household contacts.Nature immunology · 2026Article
- Harmonizing Rigidity and Flexibility: Embedding COF Quantum Dots Into Extracellular Matrix Gel as Carbon Monoxide Depot for Acoustically Triggered Time-Programmable Anti-Infective Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Structural Prediction and Functional Mechanistic Characterization of Farnesyl Diphosphate Synthase fromACS omega · 2026Article
- Restricted MHC-II trafficking inbioRxiv : the preprint server for biology · 2026Article
- IFN𝛾 and IFN𝛾 mimetics prevent IFN-I-mediated TB susceptibility by regulating iron metabolism and lipid peroxidation.bioRxiv : the preprint server for biology · 2026Article
- Does Tuberculosis Leave a Thromboinflammatory Memory After Cure? A Narrative Review with a Conceptual Framework on Hypercoagulability, Cellular Reservoirs, and Extracellular Vesicle Signaling.International journal of molecular sciences · 2026Review
- Mtb-Timer: a fluorescent reporter to visualizemSystems · 2026Article
- NRF2-mediated inhibition of alveolar macrophage MHC II expression during Mycobacterium tuberculosis infection.Cell reports · 2026Article
- Article
- Characterization of programmed cell death pathways activated in Mycobacterium tuberculosis-infected human macrophages.Cell death discovery · 2026Article
- Dual human lung models reveal compartment-specific activity of anti-tuberculosis drugs and host-directed therapies.Microbiology spectrum · 2026Article
- Mycobacterium tuberculosis preferentially infects specific macrophage subsets in primate granulomas during the early stages of tuberculosis.Mucosal immunology · 2026Article
- Inhalational therapy of pulmonary infectionActa pharmaceutica Sinica. B · 2026Article
- Deubiquitinase USP15 restricts LC3-dependent targeting ofAutophagy · 2026Article
- A temporal dialogue between the circadian clock and chronic inflammatory diseases.Disease models & mechanisms · 2026Review
- Lung organoids as a human system for Mycobacteria infection modeling and drug testing.The FEBS journal · 2026Review
- Transport Stress Induces Neuroimmune Dysregulation and Exacerbates Mycobacterium Tuberculosis Infection in Mice.International journal of molecular sciences · 2026Article
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.
Funding
Abstract
Macrophages are the primary host cell type for infection by Mycobacterium tuberculosis in vivo. Macrophages are also key immune effector cells that mediate the control of bacterial growth. However, the specific macrophage phenotypes that are required for optimal immune control of M. tuberculosis infection in vivo remain poorly defined. There are two distinct macrophage lineages in the lung, comprising embryonically derived, tissue-resident alveolar macrophages and recruited, blood monocyte-derived interstitial macrophages. Recent studies have shown that these lineages respond divergently to similar immune environments within the tuberculosis granuloma. Here, we discuss how the differing responses of macrophage lineages might affect the control or progression of tuberculosis disease. We suggest that the ability to reprogramme macrophage responses appropriately, through immunological or chemotherapeutic routes, could help to optimize vaccines and drug regimens for tuberculosis.
Indexed as
Identifiers
39774813What 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.