Evidence map›Paper›PMID 27391012›Full record

ArticlePloS one2016

A Mouse Model of Latent Tuberculosis Infection to Study Intervention Strategies to Prevent Reactivation.

Andreas Kupz, Ulrike Zedler, Manuela Stäber, Stefan H E Kaufmann

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 38 citations in OpenAlex.

  1. Applications of humanized mice inMolecular medicine reports · 2026
    Review
  2. CD8Nature communications · 2026
    Article
  3. Article
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  5. Intradermal Inoculation of Mycobacterium avium in the Mouse Ear.Journal of visualized experiments : JoVE · 2025
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Animal models for COVID-19 and tuberculosis.Frontiers in immunology · 2023
    Review
  11. Mouse Models forPathogens (Basel, Switzerland) · 2022
    Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

4 authors at 2 institutions in 2 countries.

Andreas KupzDepartment of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.
Ulrike ZedlerDepartment of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.
Manuela StäberDepartment of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.
Stefan H E KaufmannDepartment of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.ORCID http://orcid.org/0000-0001-9866-8268
Max Planck Institute for Infection Biology · DEAustralian Institute of Tropical Health and Medicine · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Infection with Mycobacterium tuberculosis (Mtb) is the leading cause of death in human immunodeficiency virus (HIV)+ individuals, particularly in Sub-Saharan Africa. Management of this deadly co-infection is a significant global health challenge that is exacerbated by the lack of efficient vaccines against both Mtb and HIV, as well as the lack of reliable and robust animal models for Mtb/HIV co-infection. Here we describe a tractable and reproducible mouse model to study the reactivation dynamics of latent Mtb infection following the loss of CD4+ T cells as it occurs in HIV-co-infected individuals. Whereas intradermally (i.d.) infected C57BL/6 mice contained Mtb within the local draining lymph nodes, depletion of CD4+ cells led to progressive systemic spread of the bacteria and induction of lung pathology. To interrogate whether reactivation of Mtb after CD4+ T cell depletion can be reversed, we employed interleukin (IL)-2/anti-IL-2 complex-mediated cell boost approaches. Although populations of non-CD4 lymphocytes, such as CD8+ memory T cells, natural killer (NK) cells and double-negative (DN) T cells significantly expanded after IL-2/anti-IL-2 complex treatment, progressive development of bacteremia and pathologic lung alterations could not be prevented. These data suggest that the failure to reverse Mtb reactivation is likely not due to anergy of the expanded cell subsets and rather indicates a limited potential for IL-2-complex-based therapies in the management of Mtb/HIV co-infection.

Indexed as

Disease Models, AnimalAnimalsCD4-Positive T-LymphocytesHumansInterleukin-2Killer Cells, NaturalLatent TuberculosisLungMiceMycobacterium tuberculosisTuberculosis, PulmonaryInterleukin-2

Identifiers

PMID27391012
PMCPMC4938611
OpenAlexW2467308937

What OpenQuestion holds

Textmetadata
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.