ReviewSeminars in immunopathology2013
Macrophages in tuberculosis: friend or foe.
Review in Seminars in immunopathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 167 papers, 3 of them syntheses that pooled it.
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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
167 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- Studying intrapulmonary pharmacokinetics for tuberculosis treatment: a systematic review of methodology.The Journal of antimicrobial chemotherapy · 2025Pooled it
- Vascular endothelial growth factor levels in tuberculosis: A systematic review and meta-analysis.PloS one · 2022Pooled it
- Spoligotyping based genetic diversity of Mycobacterium tuberculosis in Ethiopia: a systematic review.BMC infectious diseases · 2018Pooled it
- History of tuberculosis is associated with lower exhaled nitric oxide levels in HIV-infected children.AIDS (London, England) · 2019Trial
- Upper respiratory tract commensalJournal of thoracic disease · 2026Article
- Ubiquitylation by the GID/CTLH complex regulates the metabolic and innate immune response of macrophages to infection by Mycobacterium tuberculosis.PLoS pathogens · 2026Article
- Ag85A-PEGylated Propolis Nanoparticles Exhibit Intracellular Antimycobacterial and Host-Protective Activities AgainstInternational journal of molecular sciences · 2026Article
- Optimal Scale of Greenspace Exposure for Pulmonary Tuberculosis Treatment Success: Multi-scale Associations and Interactions with Air Pollutants.Journal of urban health : bulletin of the New York Academy of Medicine · 2026Article
- Type 1 diabetes alters early macrophage-iScience · 2026Article
- Mycobacterium tuberculosis MEM39 (Rv1977) hijacks host aldolase A (ALDOA) to subvert immunometabolism to facilitate bacterial intracellular survival.Cellular & molecular immunology · 2026Article
- The Sialomucin CD43 Drives Tuberculosis Immunopathology Across Different Host Genetic Backgrounds.Inflammation · 2026Article
- CD39 regulates P2RX7-mediated lung necrotic lesions in severe experimental tuberculosis.Mucosal immunology · 2026Article
- Immune endotypes in tuberculosis: Keys to decoding disease complexity.Journal of internal medicine · 2026Review
- Article
- Post-TB lung disease: pathogenesis, host-directed therapies, and the C3HeB/FeJ model for pre-clinical advances.Infection and immunity · 2026Review
- Human iPSC-derived alveolar macrophages reveal macrophage subtype functions of itaconate in M. tuberculosis defense.JCI insight · 2026Article
- Single-cell and spatial profiling highlights TB-induced myofibroblasts as drivers of lung pathology.The Journal of experimental medicine · 2026Article
- Clinical Characteristics and Prognosis of Non-Small Cell Lung Cancer with Coexisting Pulmonary Tuberculosis: A Retrospective Matched-Cohort Study.Journal of inflammation research · 2026Article
- Silymarin Reduces the Inflammatory Response and the Burden ofInternational journal of microbiology · 2026Article
- Protein-Mediated Virulence in Mycobacterium tuberculosis.Advances in experimental medicine and biology · 2026Review
107 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Tuberculosis (TB) remains one of the greatest threats to human health. The causative bacterium, Mycobacterium tuberculosis (Mtb), is acquired by the respiratory route. It is exquisitely human adapted and a prototypic intracellular pathogen of macrophages, with alveolar macrophages (AMs) being the primary conduit of infection and disease. The outcome of primary infection is most often a latently infected healthy human host, in whom the bacteria are held in check by the host immune response. Such individuals can develop active TB later in life with impairment in the immune system. In contrast, in a minority of infected individuals, the host immune response fails to control the growth of bacilli, and progressive granulomatous disease develops, facilitating spread of the bacilli via infectious aerosols coughed out into the environment and inhaled by new hosts. The molecular details of the Mtb-macrophage interaction continue to be elucidated. However, it is clear that a number of complex processes are involved at the different stages of infection that may benefit either the bacterium or the host. Macrophages demonstrate tremendous phenotypic heterogeneity and functional plasticity which, depending on the site and stage of infection, facilitate the diverse outcomes. Moreover, host responses vary depending on the specific characteristics of the infecting Mtb strain. In this chapter, we describe a contemporary view of the behavior of AMs and their interaction with various Mtb strains in generating unique immunologic lung-specific responses.
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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.