Evidence map›Paper›PMID 26075905›Full record

ArticlePloS one2015

Redundancy between Cysteine Cathepsins in Murine Experimental Autoimmune Encephalomyelitis.

Euan Ramsay Orr Allan, Robin Michael Yates

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.4field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Article
  3. Cathepsins in Neurological Diseases.International journal of molecular sciences · 2025
    Review
  4. Article
  5. Review
  6. Article
  7. Cathepsin-B inhibitor CA-074 attenuates retinopathy and optic neuritis in experimental autoimmune encephalomyelitis induced in SJL/J mice.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023
    Article
  8. Review
  9. Article
  10. Proteases, Mucus, and Mucosal Immunity in Chronic Lung Disease.International journal of molecular sciences · 2021
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Biguanide is a modifiable pharmacophore for recruitment of endogenous ZnBiometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2019
    Review
  17. Review
  18. Cathepsin H deficiency in mice induces excess Th1 cell activation and early-onset of EAE though impairment of toll-like receptor 3 cascade.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018
    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

2 authors at 1 institution in 1 country.

Euan Ramsay Orr AllanDepartment of Comparative Biology and Experimental Medicine, Faculty of Veterinary Medicine, University of Calgary, Alberta, Canada.
Robin Michael YatesDepartment of Comparative Biology and Experimental Medicine, Faculty of Veterinary Medicine, University of Calgary, Alberta, Canada; Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Calgary, Alberta, Canada.
University of Calgary · CA

Funding

Canadian Institutes of Health Research MOP-111256
6 · The paper itself

Abstract

The cysteine cathepsins B, S, and L are functionally linked to antigen processing, and hence to autoimmune disorders such as multiple sclerosis. Stemming from several studies that demonstrate that mice can be protected from experimental autoimmune encephalomyelitis (EAE) through the pharmacologic inhibition of cysteine cathepsins, it has been suggested that targeting these enzymes in multiple sclerosis may be of therapeutic benefit. Utilizing mice deficient in cysteine cathepsins both individually and in combination, we found that the myelin-associated antigen myelin oligodendrocyte glycoprotein (MOG) was efficiently processed and presented by macrophages to CD4+ T cells in the individual absence of cathepsin B, S or L. Similarly, mice deficient in cathepsin B or S were susceptible to MOG-induced EAE and displayed clinical progression and immune infiltration into the CNS, similar to their wild-type counterparts. Owing to a previously described CD4+ T cell deficiency in mice deficient in cathepsin L, such mice were protected from EAE. When multiple cysteine cathepsins were simultaneously inhibited via genetic deletion of both cathepsins B and S, or by a cathepsin inhibitor (LHVS), MHC-II surface expression, MOG antigen presentation and EAE were attenuated or prevented. This study demonstrates the functional redundancy between cathepsin B, S and L in EAE, and suggests that the inhibition of multiple cysteine cathepsins may be needed to modulate autoimmune disorders such as multiple sclerosis.

Indexed as

AnimalsAntigen PresentationCathepsinsCD4-Positive T-LymphocytesCysteineDipeptidesDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalHistocompatibility Antigens Class IIMacrophagesMaleMiceMyelin-Oligodendrocyte GlycoproteinSulfonesCathepsinsCysteineDipeptidesHistocompatibility Antigens Class IIMyelin-Oligodendrocyte GlycoproteinN-morpholinourea-leucine-homophenylalanine-phenyl-vinylsulfoneSulfones

Identifiers

PMID26075905
PMCPMC4468166
OpenAlexW1168108094

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.