Evidence map›Paper›PMID 25255101›Full record

ArticlePLoS neglected tropical diseases2014

Cathepsin B in antigen-presenting cells controls mediators of the Th1 immune response during Leishmania major infection.

Iris J Gonzalez-Leal, Bianca Röger, Angela Schwarz, Tanja Schirmeister, Thomas Reinheckel, Manfred B Lutz, Heidrun Moll

Open access · goldAbstract read
In one paragraph

Article in PLoS neglected tropical diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.2field-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

20 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Review
  3. The mycotoxin Beauvericin is an uncompetitive inhibitor of Cathepsin B.Protein science : a publication of the Protein Society · 2025
    Article
  4. Review
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  7. Review
  8. Article
  9. Article
  10. Revisiting the Principles of Designing a Vaccine.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
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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

7 authors at 3 institutions in 1 country.

Iris J Gonzalez-LealInstitute for Molecular Infection Biology, University of Würzburg, Würzburg, Germany.
Bianca RögerInstitute for Molecular Infection Biology, University of Würzburg, Würzburg, Germany.
Angela SchwarzInstitute for Molecular Infection Biology, University of Würzburg, Würzburg, Germany.
Tanja SchirmeisterUniversity of Mainz, Institute for Pharmacy and Biochemistry, Mainz, Germany.
Thomas ReinheckelUniversity of Freiburg, Institute of Molecular Medicine and Cell Research, Freiburg, Germany.
Manfred B LutzInstitute of Virology and Immunobiology, University of Würzburg, Würzburg, Germany.
Heidrun MollInstitute for Molecular Infection Biology, University of Würzburg, Würzburg, Germany.
University of Würzburg · DEJohannes Gutenberg University Mainz · DEUniversity of Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Resistance and susceptibility to Leishmania major infection in the murine model is determined by the capacity of the host to mount either a protective Th1 response or a Th2 response associated with disease progression. Previous reports involving the use of cysteine cathepsin inhibitors indicated that cathepsins B (Ctsb) and L (Ctsl) play important roles in Th1/Th2 polarization during L. major infection in both susceptible and resistant mouse strains. Although it was hypothesized that these effects are a consequence of differential patterns of antigen processing, the mechanisms underlying these differences were not further investigated. Given the pivotal roles that dendritic cells and macrophages play during Leishmania infection, we generated bone-marrow derived dendritic cells (BMDC) and macrophages (BMM) from Ctsb-/- and Ctsl-/- mice, and studied the effects of Ctsb and Ctsl deficiency on the survival of L. major in infected cells. Furthermore, the signals used by dendritic cells to instruct Th cell polarization were addressed: the expression of MHC class II and co-stimulatory molecules, and cytokine production. We found that Ctsb-/- BMDC express higher levels of MHC class II molecules than wild-type (WT) and Ctsl-/- BMDC, while there were no significant differences in the expression of co-stimulatory molecules between cathepsin-deficient and WT cells. Moreover, both BMDC and BMM from Ctsb-/- mice significantly up-regulated the levels of interleukin 12 (IL-12) expression, a key Th1-inducing cytokine. These findings indicate that Ctsb-/- BMDC display more pro-Th1 properties than their WT and Ctsl-/- counterparts, and therefore suggest that Ctsb down-regulates the Th1 response to L. major. Moreover, they propose a novel role for Ctsb as a regulator of cytokine expression.

Indexed as

AnimalsAntigen PresentationCathepsin BCathepsin LDendritic CellsDisease Models, AnimalFemaleInterleukin-12Leishmania majorLeishmaniasisMacrophagesMiceMice, Inbred BALB CMice, TransgenicTh1 CellsUp-RegulationCathepsin BCathepsin LInterleukin-12

Identifiers

PMID25255101
PMCPMC4177854
OpenAlexW2019246991

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Registered trials

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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.