Evidence map›Paper›PMID 32667673›Full record

ArticleThe Journal of experimental medicine2020

Cancer cell CCR2 orchestrates suppression of the adaptive immune response.

Miriam R Fein, Xue-Yan He, Ana S Almeida, Emilis Bružas, Arnaud Pommier, Ran Yan, Anaïs Eberhardt, Douglas T Fearon, Linda Van Aelst, John Erby Wilkinson and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 53 citations in OpenAlex.

  1. Assessment of CCR2 PET as a Biomarker for Head and Neck Squamous Cell Carcinoma.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2026
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  16. In Situ Cocktail Nanovaccine for Cancer Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    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

12 authors at 4 institutions in 3 countries.

Miriam R FeinCold Spring Harbor Laboratory, Cold Spring Harbor, NY.
Xue-Yan HeCold Spring Harbor Laboratory, Cold Spring Harbor, NY.
Ana S AlmeidaCold Spring Harbor Laboratory, Cold Spring Harbor, NY.
Emilis BružasCold Spring Harbor Laboratory, Cold Spring Harbor, NY.
Arnaud PommierCold Spring Harbor Laboratory, Cold Spring Harbor, NY.
Ran YanCold Spring Harbor Laboratory, Cold Spring Harbor, NY.
Anaïs EberhardtCold Spring Harbor Laboratory, Cold Spring Harbor, NY.
Douglas T FearonCold Spring Harbor Laboratory, Cold Spring Harbor, NY.
Linda Van AelstCold Spring Harbor Laboratory, Cold Spring Harbor, NY.
John Erby WilkinsonDepartments of Molecular and Integrative Physiology and Internal Medicine, University of Michigan, Ann Arbor, MI.
Camila O Dos SantosCold Spring Harbor Laboratory, Cold Spring Harbor, NY.
Mikala EgebladCold Spring Harbor Laboratory, Cold Spring Harbor, NY.
Cold Spring Harbor Laboratory · USCornell University · USÉcole Normale Supérieure de Lyon · FRUniversity of Michigan · US

Funding

Single-Cell Biology Shared ResourceP30CA045508 · NCI · COLD SPRING HARBOR LABORATORY · PI David A Tuveson · 1987 to 2026
$118.9M
NCI NIH HHS P30 CA045508
6 · The paper itself

Abstract

C-C chemokine receptor type 2 (CCR2) is expressed on monocytes and facilitates their recruitment to tumors. Though breast cancer cells also express CCR2, its functions in these cells are unclear. We found that Ccr2 deletion in cancer cells led to reduced tumor growth and approximately twofold longer survival in an orthotopic, isograft breast cancer mouse model. Deletion of Ccr2 in cancer cells resulted in multiple alterations associated with better immune control: increased infiltration and activation of cytotoxic T lymphocytes (CTLs) and CD103+ cross-presenting dendritic cells (DCs), as well as up-regulation of MHC class I and down-regulation of checkpoint regulator PD-L1 on the cancer cells. Pharmacological or genetic targeting of CCR2 increased cancer cell sensitivity to CTLs and enabled the cancer cells to induce DC maturation toward the CD103+ subtype. Consistently, Ccr2-/- cancer cells did not induce immune suppression in Batf3-/- mice lacking CD103+ DCs. Our results establish that CCR2 signaling in cancer cells can orchestrate suppression of the immune response.

Indexed as

Immune ToleranceAdaptive ImmunityAnimalsApoptosisB7-H1 AntigenDendritic CellsFemaleHistocompatibility Antigens Class IInterferonsMammary Neoplasms, ExperimentalMiceMice, Inbred C57BLReceptors, CCR2T-Lymphocytes, CytotoxicB7-H1 AntigenCcr2 protein, mouseCd274 protein, mouseHistocompatibility Antigens Class IInterferonsReceptors, CCR2

Identifiers

PMID32667673
PMCPMC7537399
OpenAlexW3043167974

What Socratic holds

Textmetadata
LicenceCC BY-NC-SA
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 Socratic graph.