Evidence map›Paper›PMID 19865101›Full record

ArticleGenes and immunity2010

Genetic variants of CC chemokine genes in experimental autoimmune encephalomyelitis, multiple sclerosis and rheumatoid arthritis.

J Ockinger, P Stridh, A D Beyeen, F Lundmark, M Seddighzadeh, A Oturai, P S Sørensen, A R Lorentzen, E G Celius, V Leppä and 8 more

Abstract read
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In one paragraph

Article in Genes and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. CCL13 and human diseases.Frontiers in immunology · 2023
    Review
  3. Review
  4. Article
  5. Fine-mapping QTLs in advanced intercross lines and other outbred populations.Mammalian genome : official journal of the International Mammalian Genome Society · 2014
    Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. 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

18 authors at 6 institutions in 4 countries.

J OckingerNeuroimmunology Unit, Department of Clinical Neuroscience, Center of Molecular Medicine, Karolinska Institutet, Stockholm, Sweden. johan.ockinger@ki.se
P Stridh
A D Beyeen
F Lundmark
M Seddighzadeh
A Oturai
P S Sørensen
A R Lorentzen
E G Celius
V Leppä
K Koivisto
P J Tienari
L Alfredsson
L Padyukov
J Hillert
I Kockum
M Jagodic
T Olsson
Karolinska Institutet · SEDanish Multiple Sclerosis Center · DKOslo University Hospital · NOFinnish Institute for Health and Welfare · FISeinäjoki University of Applied Sciences · FIUniversity of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is a complex disorder of the central nervous system, causing inflammation, demyelination and axonal damage. A limited number of genetic risk factors for MS have been identified, but the etiology of the disease remains largely unknown. For the identification of genes regulating neuroinflammation we used a rat model of MS, myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), and carried out a linkage analysis in an advanced intercross line (AIL). We thereby redefine the Eae18b locus to a 0.88 Mb region, including a cluster of chemokine genes. Further, we show differential expression of Ccl2, Ccl11 and Ccl11 during EAE in rat strains with opposite susceptibility to EAE, regulated by genotype in Eae18b. The human homologous genes were tested for association to MS in 3841 cases and 4046 controls from four Nordic countries. A haplotype in CCL2 and rs3136682 in CCL1 show a protective association to MS, whereas a haplotype in CCL13 is disease predisposing. In the HLA-DRB1* 15 positive subgroup, we also identified an association to a risk haplotype in CCL2, suggesting an influence from the human leukocyte antigen (HLA) locus. We further identified association to rheumatoid arthritis in CCL2, CCL8 and CCL13, indicating common regulatory mechanisms for complex diseases.

Indexed as

AnimalsArthritis, RheumatoidCentral Nervous SystemChemokinesChemokines, CCEncephalomyelitis, Autoimmune, ExperimentalGenetic LinkageGenotypeHLA-DR AntigensHLA-DRB1 ChainsHumansMiceMultiple SclerosisMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinMyelin ProteinsChemokinesChemokines, CCHLA-DR AntigensHLA-DRB1 ChainsMOG protein, humanMog protein, mouseMog protein, ratMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinMyelin Proteins

Identifiers

PMID19865101
OpenAlexW2151372018

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.