Evidence map›Paper›PMID 22144035›Full record

ArticleArthritis and rheumatism2012

Decreased Th17 and antigen-specific humoral responses in CX₃ CR1-deficient mice in the collagen-induced arthritis model.

Teresa K Tarrant, Peng Liu, Rishi R Rampersad, Denise Esserman, Lisa R Rothlein, Roman G Timoshchenko, Marcus W McGinnis, David J Fitzhugh, Dhavalkumar D Patel, Alan M Fong

Abstract read
In one paragraph

Article in Arthritis and rheumatism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
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  5. Article
  6. Article
  7. Article
  8. Tissue-specific Role of CXImmune network · 2018
    Review
  9. Dendritic cell migration in health and disease.Nature reviews. Immunology · 2017
    Review
  10. T Cell CX3CR1 Mediates Excess Atherosclerotic Inflammation in Renal Impairment.Journal of the American Society of Nephrology : JASN · 2016
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. 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

10 authors at 2 institutions in 2 countries.

Teresa K TarrantDepartment of Medicine, University of North Carolina at Chapel Hill, CB 7280, 3300 Manning Drive, Chapel Hill, NC 27599, USA. tarra002@med.unc.edu
Peng Liu
Rishi R Rampersad
Denise Esserman
Lisa R Rothlein
Roman G Timoshchenko
Marcus W McGinnis
David J Fitzhugh
Dhavalkumar D Patel
Alan M Fong
University of North Carolina at Chapel Hill · USNovartis Institutes for BioMedical Research

Funding

Role of CX3CR1 in the Pathogenesis of AtherosclerosisR01HL077406 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI FONG, ALAN M · 2006 to 2010
$1.8M
G Protein Coupled Receptor Regulatory Mechanisms in ArthritisK08AI070684 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI TARRANT, TERESA KATHLEEN · 2006 to 2010
$527k
NHLBI NIH HHS R01 HL077406NHLBI NIH HHS R01-HL-077406NIAID NIH HHS K08 AI070684NIAID NIH HHS K08-AI-070684
6 · The paper itself

Abstract

objectiveCX(3) CR1 is a chemokine receptor that uniquely binds to its ligand fractalkine (CX(3) CL1) and has been shown to be important in inflammatory arthritis responses, largely due to its effects on cellular migration. This study was undertaken to test the hypothesis that genetic deficiency of CX(3) CR1 is protective in the chronic inflammatory arthritis model collagen-induced arthritis (CIA). Because CX(3) CR1 is expressed on T cells and antigen-presenting cells, we also examined adaptive immune functions in this model.

methodsAutoantibody formation, clinical, histologic, T cell proliferative, and cytokine responses were evaluated in wild-type and CX(3) CR1-deficient DBA/1J mice after immunization with heterologous type II collagen (CII).

resultsCX(3) CR1(-/-) mice had an ∼30% reduction in arthritis severity compared to wild-type mice, as determined by 2 independent measures, paw swelling (P < 0.01) and clinical disease score (P < 0.0001). Additionally, compared to wild-type mice, CX(3) CR1(-/-) mice had an ∼50% decrease in anti-CII autoantibody formation (P < 0.05), decreased Th17 intraarticular cytokine expression (P < 0.01 for interleukin-17 [IL-17] and P < 0.001 for IL-23), and decreased total numbers of Th17 cells in inflamed joints (P < 0.05).

conclusionOur findings indicate that CX(3) CR1 deficiency is protective in inflammatory arthritis and may have effects that extend beyond migration that involve adaptive immune responses in autoimmune disease.

Indexed as

Adaptive ImmunityAnimalsArthritis, ExperimentalCell MovementCX3C Chemokine Receptor 1Disease ProgressionHindlimbImmunity, HumoralMaleMiceMice, Inbred DBAMice, KnockoutReceptors, ChemokineStifleTh17 CellsCX3C Chemokine Receptor 1Cx3cr1 protein, mouseReceptors, Chemokine

Identifiers

PMID22144035
PMCPMC3238788
OpenAlexW2065023235

What OpenQuestion holds

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LicenceTDM
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.