Evidence map›Paper›PMID 26438324›Full record

ReviewSeminars in immunopathology2016

Pathology and immune reactivity: understanding multidimensionality in pulmonary tuberculosis.

Anca Dorhoi, Stefan H E Kaufmann

Abstract readReview
PubMed Publisher
In one paragraph

Review in Seminars in immunopathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
8.0field-weighted citation impact, top 2% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

77 citing papers in PubMed, 144 citations in OpenAlex.

  1. Trial
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  11. Plasma cytokine levels as markers of pathogenesis and treatment response in patients with non-tuberculous mycobacterial pulmonary disease.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024
    Article
  12. Article
  13. Review
  14. Article
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  16. Gasdermin D kills bacteria.Microbiological research · 2023
    Review
  17. iScience · 2023
    Review
  18. Article
  19. Review
  20. Tuberculosis: Pathogenesis, Current Treatment Regimens and New Drug Targets.International journal of molecular sciences · 2023
    Review

17 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Anca DorhoiDepartment of Immunology, Max Planck Institute for Infection Biology, Charitéplatz 1, 10117, Berlin, Germany. dorhoi@mpiib-berlin.mpg.de.
Stefan H E KaufmannDepartment of Immunology, Max Planck Institute for Infection Biology, Charitéplatz 1, 10117, Berlin, Germany. kaufmann@mpiib-berlin.mpg.de.
Charité - Universitätsmedizin Berlin · DEMax Planck Institute for Infection Biology · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heightened morbidity and mortality in pulmonary tuberculosis (TB) are consequences of complex disease processes triggered by the causative agent, Mycobacterium tuberculosis (Mtb). Mtb modulates inflammation at distinct stages of its intracellular life. Recognition and phagocytosis, replication in phagosomes and cytosol escape induce tightly regulated release of cytokines [including interleukin (IL)-1, tumor necrosis factor (TNF), IL-10], chemokines, lipid mediators, and type I interferons (IFN-I). Mtb occupies various lung lesions at sites of pathology. Bacteria are barely detectable at foci of lipid pneumonia or in perivascular/bronchiolar cuffs. However, abundant organisms are evident in caseating granulomas and at the cavity wall. Such lesions follow polar trajectories towards fibrosis, encapsulation and mineralization or liquefaction, extensive matrix destruction, and tissue injury. The outcome is determined by immune factors acting in concert. Gradients of cytokines and chemokines (CCR2, CXCR2, CXCR3/CXCR5 agonists; TNF/IL-10, IL-1/IFN-I), expression of activation/death markers on immune cells (TNF receptor 1, PD-1, IL-27 receptor) or abundance of enzymes [arginase-1, matrix metalloprotease (MMP)-1, MMP-8, MMP-9] drive genesis and progression of lesions. Distinct lesions coexist such that inflammation in TB encompasses a spectrum of tissue changes. A better understanding of the multidimensionality of immunopathology in TB will inform novel therapies against this pulmonary disease.

Indexed as

Host-Pathogen InteractionsAnimalsGranulomaHumansImmune SystemLungMycobacterium tuberculosisNecrosisTuberculosis, PulmonaryCavitationGranulomaInflammationLungMycobacterium tuberculosis

Identifiers

PMID26438324
OpenAlexW2181175475

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.