Evidence map›Paper›PMID 26542392›Full record

ReviewSeminars in immunopathology2016

Mouse models of human TB pathology: roles in the analysis of necrosis and the development of host-directed therapies.

Igor Kramnik, Gillian Beamer

Open access · hybridAbstract readReview
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 114 papers.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed
9.1field-weighted citation impact, top 1% 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

114 citing papers in PubMed, 173 citations in OpenAlex.

  1. Article
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  5. bioRxiv : the preprint server for biology · 2026
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  11. Review
  12. AFrontiers in tuberculosis · 2026
    Article
  13. Novel Multistage SubunitVaccines · 2025
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  15. Article
  16. Article
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  19. bioRxiv : the preprint server for biology · 2025
    Article
  20. Article

54 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.

Igor KramnikPulmonary Center, Department of Medicine, National Emerging Infectious Diseases Laboratories, Boston University School of Medicine, 620 Albany Street, Room 501, Boston, MA, 02118, USA. ikramnik@bu.edu.
Gillian BeamerDepartment of Infectious Disease and Global Health, Cummings School of Veterinary Medicine, Tufts University, 200 Westboro Rd, Bldg 20, Grafton, MA, 01536, USA. Gillian.Beamer@tufts.edu.
Boston University · USTufts University · US

Funding

Necrosis in pulmonary TB granulomas: dynamics, mechanisms, therapiesR01HL126066 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI KRAMNIK, IGOR, NIEDERWEIS, MICHAEL · 2016 to 2025
$5.6M
Genetics of Host Resistance &Susceptibility to TBR01HL059836 · NHLBI · YESHIVA UNIVERSITY · PI KRAMNIK, IGOR · 1997 to 2012
$4.3M
Novel TB Treatment Strategy - Optimization of Macrophage Responsiveness to IFNyR33AI105944 · NIAID · BOSTON UNIVERSITY MEDICAL CAMPUS · PI KRAMNIK, IGOR · 2015 to 2017
$1.5M
NHLBI NIH HHS R01 HL059836NHLBI NIH HHS R01 HL126066NIAID NIH HHS R33 AI105944
6 · The paper itself

Abstract

A key aspect of TB pathogenesis that maintains Mycobacterium tuberculosis in the human population is the ability to cause necrosis in pulmonary lesions. As co-evolution shaped M . tuberculosis (M.tb) and human responses, the complete TB disease profile and lesion manifestation are not fully reproduced by any animal model. However, animal models are absolutely critical to understand how infection with virulent M.tb generates outcomes necessary for the pathogen transmission and evolutionary success. In humans, a wide spectrum of TB outcomes has been recognized based on clinical and epidemiological data. In mice, there is clear genetic basis for susceptibility. Although the spectra of human and mouse TB do not completely overlap, comparison of human TB with mouse lesions across genetically diverse strains firmly establishes points of convergence. By embracing the genetic heterogeneity of the mouse population, we gain tremendous advantage in the quest for suitable in vivo models. Below, we review genetically defined mouse models that recapitulate a key element of M.tb pathogenesis-induction of necrotic TB lesions in the lungs-and discuss how these models may reflect TB stratification and pathogenesis in humans. The approach ensures that roles that mouse models play in basic and translational TB research will continue to increase allowing researchers to address fundamental questions of TB pathogenesis and bacterial physiology in vivo using this well-defined, reproducible, and cost-efficient system. Combination of the new generation mouse models with advanced imaging technologies will also allow rapid and inexpensive assessment of experimental vaccines and therapies prior to testing in larger animals and clinical trials.

Indexed as

Host-Pathogen InteractionsAnimalsAntitubercular AgentsDisease Models, AnimalGenetic LociGenetic Predisposition to DiseaseGenetic VariationGranulomaHumansMacrophagesMiceMycobacterium tuberculosisNecrosisNeutrophilsReceptors, SomatostatinTuberculosisAntitubercular AgentsReceptors, Somatostatinsomatostatin receptor 1, mouseAnimal modelsGranulomaHost-directed therapiesInbred miceMechanismsNecrosissst1Tuberculosis

Identifiers

PMID26542392
PMCPMC4779126
OpenAlexW2130124733

What OpenQuestion holds

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LicenceCC BY
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.