Evidence map›Paper›PMID 26834705›Full record

ArticleFrontiers in microbiology2015

Fatal Leishmaniasis in the Absence of TNF Despite a Strong Th1 Response.

Phillip D Fromm, Jessica C Kling, Annika Remke, Christian Bogdan, Heinrich Körner

Open access · goldAbstract read
In one paragraph

Article in Frontiers in microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
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  4. Article
  5. Review
  6. The role of CD4Frontiers in cellular and infection microbiology · 2024
    Review
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  8. Pathogens (Basel, Switzerland) · 2023
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Selective Targeting of TNF Receptors as a Novel Therapeutic Approach.Frontiers in cell and developmental biology · 2020
    Review
  17. Article
  18. Article
  19. Article
  20. Article
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

5 authors at 4 institutions in 2 countries.

Phillip D FrommComparative Genomics Centre, James Cook University, Townsville QN, Australia.
Jessica C KlingMenzies Institute for Medical Research Tasmania, HobartTAS, Australia; Blumenthal Group, The University of Queensland Diamantina Institute, Translational Research Institute, WoolloongabbaQLD, Australia.
Annika RemkeMenzies Institute for Medical Research Tasmania, Hobart TAS, Australia.
Christian BogdanMikrobiologisches Institut - Klinische Mikrobiologie, Immunologie und Hygiene, Friederich-Alexander-Universität Erlangen-Nürnberg, Universitätsklinikum Erlangen Erlangen, Germany.
Heinrich KörnerMenzies Institute for Medical Research Tasmania, Hobart TAS, Australia.
Menzies Institute for Medical ResearchJames Cook University · AUUniversitätsklinikum Erlangen · DEUniversity of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Induction of inducible nitric oxide synthase in mononuclear phagocytes by IFN-γ and innate tumor necrosis factor (TNF) provide the basis for an effective immune response to the intracellular parasite Leishmania (L.) major. In previous experiments, we observed a fatal visceral form of leishmaniasis in L. major-infected C57BL/6 TNF(-/-) mice. To further delineate the protective function of TNF and its receptor requirements, we comparatively assessed L. major-infected C57BL/6 mice that were either deficient for membrane and soluble TNF (Tnf (-) (/) (-)), for soluble TNF alone (memTnf(Δ/Δ) ), or the TNF receptors type 1 (Tnfr1 (-) (/) (-)) or type 2 (Tnfr2 (-) (/) (-)). We detected locally and systemically increased levels of the cytokine IFN-γ in the absence of the TNF-TNFR1-signaling pathway. An analysis of transcription factors and cytokines revealed that activated Tnf (-) (/) (-) CD4(+) T cells displayed a highly active Th1 phenotype with a strong usage of the T cell receptor Vβ5.1/2. From these data we conclude that the fatal outcome of L. major infection in Tnf (-) (/) (-) mice does not result from a skewed or deficient Th1 differentiation.

Indexed as

cutaneous leishmaniasisIFN-γmouse modelsT cell subtypestumor necrosis factor

Identifiers

PMID26834705
PMCPMC4722107
OpenAlexW2267343775

What OpenQuestion holds

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LicenceCC BY
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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.