ReviewCold Spring Harbor perspectives in medicine2014
Immunity and Immunopathology in the Tuberculous Granuloma.
Review in Cold Spring Harbor perspectives in medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 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
105 citing papers in PubMed, 189 citations in OpenAlex.
- Antigen Availability Shapes T Cell Differentiation and Function during Tuberculosis.Cell host & microbe · 2017Trial
- Circulating Angiogenic Factors as Biomarkers of Disease Severity and Bacterial Burden in Pulmonary Tuberculosis.PloS one · 2016Trial
- Article
- The Proteome of Plasma Extracellular Vesicles in Latent and Active Tuberculosis Reveals Phase-Specific Composition and Immunometabolic Insights.FASEB bioAdvances · 2026Article
- An unusual presentation of miliary tuberculosis with medullary nephrocalcinosis in an infant.Radiology case reports · 2026Article
- Macrophage adaptation to hypoxia in the tuberculous granuloma potentiates mycobacterium-induced mitochondrial damage and granuloma necrosis.bioRxiv : the preprint server for biology · 2026Article
- Macrophage states and polarization duringFrontiers in cellular and infection microbiology · 2026Review
- CDK1‑induced regulation of p53 phosphorylation at Ser315 mediates cell cycle arrest and apoptosis of macrophages infected with clinical isolates ofMolecular medicine reports · 2026Article
- Transcriptomic insights intoThe veterinary quarterly · 2025Article
- Immunopathogenesis of tuberculosis: cellular mechanisms and immune modulation.Veterinary research · 2025Review
- Early and opposing neutrophil and CD4 T cell responses shape pulmonary tuberculosis pathology.The Journal of experimental medicine · 2025Article
- Serum metabolic disparity between patients with lymph node tuberculosis and patients with sarcoidosis: towards differential diagnosis.BMC pulmonary medicine · 2025Article
- Host-intrinsic and host-extrinsic factors modulate immunity to Mtb infection, reinfection, and noncanonical vaccination routes.Cell reports. Medicine · 2025Review
- A granulin-positive macrophage subtype in mycobacterial granulomas alleviates tissue damage by limiting excessive inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Granulysin Antimicrobial Activity Promotes Dormancy in Mycobacterium tuberculosis.European journal of immunology · 2025Article
- Adjunctive beneficial effect of c-di-GMP, a STING agonist, in enhancing protective efficacy of TLR4-adjuvanted tuberculosis subunit vaccine formulations.Journal of biomedical science · 2025Article
- Review
- Soluble immune mediators orchestrate protectiveeLife · 2025Article
- Association Between 10 Autoimmune Diseases and Risk of Pulmonary Tuberculosis: A Mendelian Randomization Study.Journal of multidisciplinary healthcare · 2025Article
- Review
45 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Granulomas, organized aggregates of immune cells, are a defining feature of tuberculosis (TB). Granuloma formation is implicated in the pathogenesis of a variety of inflammatory disorders. However, the tuberculous granuloma has been assigned the role of a host protective structure which "walls-off" mycobacteria. Work conducted over the past decade has provided a more nuanced view of its role in pathogenesis. On the one hand, pathogenic mycobacteria accelerate and exploit granuloma formation for their expansion and dissemination by manipulating host immune responses to turn leukocyte recruitment and cell death pathways in their favor. On the other hand, granuloma macrophages can preserve granuloma integrity by exerting a microbicidal immune response, thus preventing an even more rampant expansion of infection in the extracellular milieu. Even this host-beneficial immune response required to maintain the bacteria intracellular must be tempered, as an overly vigorous immune response can also cause granuloma breakdown, thereby directly supporting bacterial growth extracellularly. This review will discuss how mycobacteria manipulate inflammatory responses to drive granuloma formation and will consider the roles of the granuloma in pathogenesis and protective immunity, drawing from clinical studies of TB in humans and from animal models--rodents, zebrafish, and nonhuman primates. A deeper understanding of TB pathogenesis and immunity in the granuloma could suggest therapeutic approaches to abrogate the host-detrimental aspects of granuloma formation to convert it into the host-beneficial structure that it has been thought to be for nearly a century.
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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.