Evidence map›Paper›PMID 24706865›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Pharmacological inhibition of the chemokine receptor CX3CR1 attenuates disease in a chronic-relapsing rat model for multiple sclerosis.

Anna Ridderstad Wollberg, Anders Ericsson-Dahlstrand, Anders Juréus, Petra Ekerot, Sylvia Simon, Maria Nilsson, Stig-Johan Wiklund, Anna-Lena Berg, Mats Ferm, Dan Sunnemark and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

62 citing papers in PubMed, 92 citations in OpenAlex.

  1. The CX3CL1-CX3CR1 axis in HIV-associated inflammation and cardiometabolic disease.American journal of physiology. Regulatory, integrative and comparative physiology · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Research (Washington, D.C.) · 2025
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Dysregulated NFrontiers of medicine · 2024
    Article
  18. Article
  19. Fractalkine Signalling (CXJournal of clinical medicine · 2023
    Review
  20. CXInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article

2 more citing papers are in PubMed but not listed here.

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

11 authors at 1 institution in 1 country.

Anna Ridderstad WollbergInnovative Medicines, CNS and Pain Control, AstraZeneca R&D Södertälje, SE-151 85 Södertälje, Sweden.
Anders Ericsson-Dahlstrand
Anders Juréus
Petra Ekerot
Sylvia Simon
Maria Nilsson
Stig-Johan Wiklund
Anna-Lena Berg
Mats Ferm
Dan Sunnemark
Rolf Johansson
AstraZeneca (Sweden) · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

One hallmark of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) is infiltration of leukocytes into the CNS, where chemokines and their receptors play a major mediatory role. CX3CR1 is a chemokine receptor involved in leukocyte adhesion and migration and hence a mediator of immune defense reactions. The role of CX3CR1 in MS and EAE pathogenesis however remains to be fully assessed. Here, we demonstrate CX3CR1 mRNA expression on inflammatory cells within active plaque areas in MS brain autopsies. To test whether blocking CNS infiltration of peripheral leukocytes expressing CX3CR1 would be a suitable treatment strategy for MS, we developed a selective, high-affinity inhibitor of CX3CR1 (AZD8797). The compound is active outside the CNS and AZD8797 treatment in Dark Agouti rats with myelin oligodendrocyte glycoprotein-induced EAE resulted in reduced paralysis, CNS pathology, and incidence of relapses. The compound is effective when starting treatment before onset, as well as after the acute phase. This treatment strategy is mechanistically similar to, but more restricted than, current very late antigen-4-directed approaches that have significant side effects. We suggest that blocking CX3CR1 on leukocytes outside the CNS could be an alternative approach to treat MS.

Indexed as

Disease Models, AnimalAnimalsBrainChronic DiseaseCX3C Chemokine Receptor 1Multiple SclerosisRatsReceptors, ChemokineRecurrenceCX3C Chemokine Receptor 1CX3CR1 protein, ratReceptors, Chemokinefractalkine receptorinflammation

Identifiers

PMID24706865
PMCPMC3986185
OpenAlexW2077943662

What OpenQuestion holds

Textmetadata
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.