Evidence map›Paper›PMID 20506316›Full record

ArticleArthritis and rheumatism2010

Deficiency of CXCR2, but not other chemokine receptors, attenuates autoantibody-mediated arthritis in a murine model.

Jonathan P Jacobs, Adriana Ortiz-Lopez, James J Campbell, Craig J Gerard, Diane Mathis, Christophe Benoist

Abstract read
In one paragraph

Article in Arthritis and rheumatism, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

65 citing papers in PubMed, 105 citations in OpenAlex.

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  2. p75Science advances · 2026
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  20. IL-4 controls activated neutrophil FcγR2b expression and migration into inflamed joints.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article

5 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

6 authors at 3 institutions in 1 country.

Jonathan P JacobsBrigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
Adriana Ortiz-Lopez
James J Campbell
Craig J Gerard
Diane Mathis
Christophe Benoist
Brigham and Women's Hospital · USBoston Children's Hospital · USHarvard University · US

Funding

Genetics of arthritis suscuptibility in outbred HS miceR01AR055271 · NIAMS · JOSLIN DIABETES CENTER · PI BENOIST, CHRISTOPHE O. · 2007 to 2011
$1.8M
Howard Hughes Medical InstituteNIAMS NIH HHS R01 AR055271NIAMS NIH HHS R01-AR-055271
6 · The paper itself

Abstract

objectiveChemokines coordinate leukocyte trafficking in homeostasis and during immune responses. Prior studies of their role in arthritis have used animal models with both an initial adaptive immune response and an inflammatory effector phase. We undertook analysis of chemokines and their receptors in the effector phase of arthritis using the K/BxN mouse serum-transfer model.

methodsA time-course microarray analysis of serum-transferred arthritis was performed, examining ankle tissue, synovial fluid, and peripheral blood leukocytes. Up-regulation of chemokines was confirmed by quantitative reverse transcriptase-polymerase chain reaction. The functional relevance of chemokine induction was assessed by transferring serum into mice deficient in CCR1-7, CCR9, CXCR2, CXCR3, CXCR5, CX(3)CR1, CCL2, or CCL3. Further mechanistic analysis of CXCR2 involved treatment of arthritic mice with a CXCR2 antagonist, bone marrow (BM) cell transfers with CXCR2(+/-) and CXCR2(-/-) donors and recipients, flow cytometry of synovial cells, and competition experiments measuring enrichment of CXCR2-expressing neutrophils in arthritic joints of mice with mixed CXCR2(+/+) and CXCR2(-/-) BM cells.

resultsGene expression profiling revealed up-regulation of the CXCR2 ligands CXCL1, CXCL2, and CXCL5 in the joint in parallel with disease activity. CXCR2(-/-) mice had attenuated disease relative to CXCR2(+/-) littermates, as did mice receiving the CXCR2 inhibitor, while deficiency of other chemokine receptors did not affect arthritis severity. CXCR2 was required only on hematopoietic cells and was widely expressed on synovial neutrophils. CXCR2-expressing neutrophils were preferentially recruited to arthritic joints in the presence of CXCR2-deficient neutrophils.

conclusionCXCR2 (but not other chemokine receptors) is critical for the development of autoantibody-mediated arthritis, exhibiting a cell-autonomous role in neutrophil recruitment to inflamed joints.

Indexed as

Up-RegulationAnimalsArthritis, ExperimentalChemokinesFemaleGene Expression ProfilingJointsMaleMiceMice, Inbred BALB CMice, Inbred NODMice, KnockoutMicroarray AnalysisNeutrophil InfiltrationNeutrophilsReceptors, Interleukin-8BChemokinesReceptors, Interleukin-8B

Identifiers

PMID20506316
PMCPMC2994550
OpenAlexW1491832748

What OpenQuestion holds

Textmetadata
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.