Evidence map›Paper›PMID 28827539›Full record

ArticleScientific reports2017

T cell specific Cxcr5 deficiency prevents rheumatoid arthritis.

Georgios L Moschovakis, Anja Bubke, Michaela Friedrichsen, Christine S Falk, Regina Feederle, Reinhold Förster

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

37 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. T cells in health and disease.Signal transduction and targeted therapy · 2023
    Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. In Vivo Imaging of Tfh Cells.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  15. Review
  16. Review
  17. Review
  18. Review
  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

6 authors at 2 institutions in 1 country.

Georgios L MoschovakisInstitute of Immunology, Hannover Medical School, Carl-Neuberg Str. 1, 30625, Hannover, Germany. Moschovakis.Leandros@mh-hannover.de.
Anja BubkeInstitute of Immunology, Hannover Medical School, Carl-Neuberg Str. 1, 30625, Hannover, Germany.
Michaela FriedrichsenInstitute of Immunology, Hannover Medical School, Carl-Neuberg Str. 1, 30625, Hannover, Germany.
Christine S FalkInstitute of Transplant Immunology, Integrated Research and Treatment Center Transplantation, IFB.Tx, Hannover Medical School, Carl-Neuberg Str. 1, 30625, Hannover, Germany.
Regina FeederleInstitute for Diabetes and Obesity, Monoclonal Antibody Core Facility and Research Group, Helmholtz Center Munich, German Research Center for Environmental Health (GmbH), Marchioninistr. 25, 81377, Munich, Germany.
Reinhold FörsterInstitute of Immunology, Hannover Medical School, Carl-Neuberg Str. 1, 30625, Hannover, Germany. Foerster.Reinhold@mh-hannover.de.
Medizinische Hochschule Hannover · DEGerman Center for Diabetes Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The chemokine receptor CXCR5 is primarily expressed on B cells and Tfh cells and facilitates their migration towards B cell follicles. In the present study we investigated the role of the CXCL13/CXCR5 axis in the pathogenesis of rheumatoid arthritis (RA) and specifically addressed the impact of CXCR5-mediated T and B cell migration in this disease. Employing collagen-induced arthritis (CIA) we identify CXCR5 as an absolutely essential factor for the induction of inflammatory autoimmune arthritis. Cxcr5-deficient mice and mice selectively lacking Cxcr5 on T cells were completely resistant to CIA, showed impaired germinal center responses and failed to mount an IgG1 antibody response to collagen II. Selective ablation of CXCR5 expression in B cells also led to suppression of CIA owing to diminished GC responses in secondary lymphoid organs (SLO) and impaired anti-collagen II antibody production. Chimeric mice harboring Cxcr5-proficient and Cxcr5-deficient immune cells revealed SLO and not the synovial tissue as the compartment where CXCR5-mediated cell migration induces autoimmune inflammation in arthritis. Thus our data demonstrate that CXCR5-mediated co-localization of Tfh cells and B cells in SLOs is absolutely essential for the induction of RA and identify CXCR5 and Tfh cells as promising therapeutic targets for the treatment of RA.

Indexed as

AnimalsArthritis, RheumatoidB-LymphocytesDisease Models, AnimalDisease SusceptibilityHumansLeukocytesMiceMice, KnockoutOrgan SpecificityPhenotypeReceptors, CXCR5T-Lymphocyte SubsetsCXCR5 protein, humanReceptors, CXCR5

Identifiers

PMID28827539
PMCPMC5567121
OpenAlexW2745455763

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.