Evidence map›Paper›PMID 21680896›Full record

ArticleCirculation research2011

Genetic deletion of chemokine receptor Ccr6 decreases atherogenesis in ApoE-deficient mice.

Wuzhou Wan, Jean K Lim, Michail S Lionakis, Aymeric Rivollier, David H McDermott, Brian L Kelsall, Joshua M Farber, Philip M Murphy

Open access · bronzeAbstract read
In one paragraph

Article in Circulation research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.8field-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

29 citing papers in PubMed, 56 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Wuzhou WanLaboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Jean K Lim
Michail S Lionakis
Aymeric Rivollier
David H McDermott
Brian L Kelsall
Joshua M Farber
Philip M Murphy
National Institute of Allergy and Infectious Diseases · US

Funding

Molecular Analysis Of Leukocyte Activation By ChemoattractantsZIAAI000615 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MURPHY, PHILIP · 2009 to 2025
$44.8M
Antigen Processing And Presentation In The IntestineZIAAI000833 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI KELSALL, BRIAN · 2009 to 2025
$24.9M
Characterization Of Novel Chemokine Receptors In LymphocytesZIAAI000749 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI FARBER, JOSHUA M · 2009 to 2011
$4.0M
Intramural NIH HHS ZIA AI000615
6 · The paper itself

Abstract

rationaleThe chemokine receptor Ccr6 is a G-protein-coupled receptor expressed on various types of leukocytes identified in mouse atherosclerotic lesions. Recent evidence suggests that both CCR6 and its ligand CCL20 are also present in human atheroma; however, their functional roles in atherogenesis remain undefined.

objectiveOur objective was to delineate the role of Ccr6 in atherogenesis in the apolipoprotein E-deficient (ApoE(-/-)) mouse model of atherosclerosis. METHODS AND

resultsBoth Ccr6 and Ccl20 are expressed in atherosclerotic aorta from ApoE(-/-) mice. Aortic lesion area in Ccr6(-/-)ApoE(-/-) mice was ∼40% and ∼30% smaller than in Ccr6(+/+)ApoE(-/-) mice at 16 and 24 weeks of age, respectively. Transplantation of bone marrow from Ccr6(-/-) mice into ApoE(-/-) mice resulted in ∼40% less atherosclerotic lesion area than for bone marrow from Ccr6(+/+) mice; lesions in Ccr6(-/-)ApoE(-/-) mice had 44% less macrophage content than lesions in Ccr6(+/+)ApoE(-/-) mice. Ccr6 was expressed on a subset of primary mouse monocytes. Accordingly, Ccl20 induced chemotaxis of primary monocytes from wild-type but not Ccr6(-/-) mice; moreover, Ccl20 induced monocytosis in ApoE(-/-) mice in vivo. Consistent with this, we observed 30% fewer monocytes in circulating blood of Ccr6(-/-)ApoE(-/-) mice, mainly because of fewer CD11b(+)Ly6C(high) inflammatory monocytes.

conclusionsCcr6 promotes atherosclerosis in ApoE-deficient mice, which may be due in part to Ccr6 support of normal monocyte levels in blood, as well as direct Ccr6-dependent monocyte migration.

Indexed as

Gene DeletionAnimalsAntigens, LyAortaAortic DiseasesApolipoproteins EAtherosclerosisBone Marrow TransplantationCD11b AntigenCell LineChemokine CCL20Chemotaxis, LeukocyteDisease Models, AnimalFemaleLeukocyte CountMacrophagesAntigens, LyApolipoproteins ECCL20 protein, mouseCCR6 protein, mouseCD11b AntigenChemokine CCL20Ly-6C antigen, mouseReceptors, CCR6

Identifiers

PMID21680896
PMCPMC3151346
OpenAlexW2116474506

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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.