Evidence map›Paper›PMID 9366570›Full record

ArticleThe Journal of clinical investigation1997

Impaired monocyte migration and reduced type 1 (Th1) cytokine responses in C-C chemokine receptor 2 knockout mice.

L Boring, J Gosling, S W Chensue, S L Kunkel, R V Farese, H E Broxmeyer, I F Charo

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 455 papers.

0numbers the graph read from it
0cells of the map it votes in
455citing papers in PubMed
18.4field-weighted citation impact, top 1% 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

455 citing papers in PubMed, 1,091 citations in OpenAlex.

  1. Trial
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  4. CD4Science (New York, N.Y.) · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Human peritoneal CCR2Human cell · 2026
    Article
  9. Monocyte Chemokines Enhance Atherosclerotic Plaque Necrosis After Bacterial Kidney Infection.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  10. Article
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  12. Article
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  15. Review
  16. Article
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395 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

7 authors at 3 institutions in 2 countries.

L BoringGladstone Institute of Cardiovascular Disease, University of California, San Francisco 94141-9100, USA.
J Gosling
S W Chensue
S L Kunkel
R V Farese
H E Broxmeyer
I F Charo
University of California, San Francisco · USUniversity Medical Center · USUniversity of Michigan–Ann Arbor · US

Funding

MECHANISMS OF SYNERGISTIC REGULATION OF STEM/PROGENITORSR01HL056416 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI BROXMEYER, HAL E. · 1996 to 2017
$6.0M
STRUCTURE AND FUNCTION OF THE MONOCYTE MCP-1 RECEPTORR01HL052773 · NHLBI · J. DAVID GLADSTONE INSTITUTES · PI CHARO, ISRAEL F. · 1994 to 2010
$5.7M
CHEMOKINES/CYTOKINES AND RECEPTORS IN STEM CELL HOMINGR01DK053674 · NIDDK · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI BROXMEYER, HAL E. · 1997 to 2005
$1.6M
NHLBI NIH HHS HL-52773NHLBI NIH HHS HL-56416NIDDK NIH HHS DK-53674
6 · The paper itself

Abstract

Monocyte chemoattractant protein-1 (MCP-1) is a potent agonist for mononuclear leukocytes and has been implicated in the pathogenesis of atherosclerosis and granulomatous lung disease. To determine the role of MCP-1 and related family members in vivo, we used homologous recombination in embryonic stem cells to generate mice with a targeted disruption of C-C chemokine receptor 2 (CCR2), the receptor for MCP-1. CCR2-/- mice were born at the expected Mendelian ratios and developed normally. In response to thioglycollate, the recruitment of peritoneal macrophages decreased selectively. In in vitro chemotaxis assays, CCR2-/- leukocytes failed to migrate in response to MCP-1. Granulomatous lung disease was induced in presensitized mice by embolization with beads coupled to purified protein derivative (PPD) of Mycobacterium bovis. As compared with wild-type littermates, CCR2-/- mice had a decrease in granuloma size accompanied by a dramatic decrease in the level of interferon gamma in the draining lymph nodes. Production of interferon gamma was also decreased in PPD-sensitized splenocytes from CCR2-/- mice and in naive splenocytes activated by concanavalin A. We conclude that CCR2-/- mice have significant defects in both delayed-type hypersensitivity responses and production of Th1-type cytokines. These data suggest an important and unexpected role for CCR2 activation in modulating the immune response, as well as in recruiting monocytes/macrophages to sites of inflammation.

Indexed as

AnimalsBone Marrow CellsChemokine CCL2ChemokinesChemotaxis, LeukocyteCytokinesEmbryo, MammalianGranuloma, Respiratory TractHematopoietic Stem CellsHumansLung DiseasesLymph NodesMacrophages, AlveolarMiceMice, KnockoutMonocytesCCR2 protein, humanCcr2 protein, mouseChemokine CCL2ChemokinesCytokinesReceptors, CCR2Receptors, CCR5Receptors, ChemokineRecombinant ProteinsTuberculin

Identifiers

PMID9366570
PMCPMC508456
OpenAlexW2133793569

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.