Evidence map›Paper›PMID 19864606›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2009

Chemokine-like receptor-1 expression by central nervous system-infiltrating leukocytes and involvement in a model of autoimmune demyelinating disease.

Kareem L Graham, Brian A Zabel, Sanam Loghavi, Luis A Zuniga, Peggy P Ho, Raymond A Sobel, Eugene C Butcher

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

47 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Chemerin triggers migration of a CD8 T cell subset with natural killer cell functions.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  5. The Role of Adipokines in the Pathologies of the Central Nervous System.International journal of molecular sciences · 2023
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Adipokines as Immune Cell Modulators in Multiple Sclerosis.International journal of molecular sciences · 2021
    Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. DGAT1 inhibits retinol-dependent regulatory T cell formation and mediates autoimmune encephalomyelitis.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  19. Article
  20. Review
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 2 institutions in 1 country.

Kareem L GrahamDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA. kareem.graham@stanford.edu
Brian A Zabel
Sanam Loghavi
Luis A Zuniga
Peggy P Ho
Raymond A Sobel
Eugene C Butcher
Stanford University · USVA Palo Alto Health Care System · US

Funding

MOLECULAR &CELLULAR IMMUNOBIOLOGYT32AI007290 · NIAID · STANFORD UNIVERSITY · PI Sean Curtis Bendall, Olivia M Martinez · 1985 to 2026
$27.0M
SCOR in Cellular and Molecular Mechanisms of AsthmaP50HL067674 · NHLBI · STANFORD UNIVERSITY · PI VAN DE RIJN, JAN MATT · 2002 to 2005
$4.8M
Intestinal Lymphocyte TraffickingR01AI047822 · NIAID · STANFORD UNIVERSITY · PI EUGENE C BUTCHER · 2001 to 2026
$4.7M
Intestinal Lymphocyte TraffickingR37AI047822 · NIAID · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI BUTCHER, EUGENE C · 2011 to 2020
$3.5M
ENDOTHELIAL CELL BIOLOGY IN INFLAMMATIONR37GM037734 · NIGMS · STANFORD UNIVERSITY · PI BUTCHER, EUGENE C · 1999 to 2008
$2.8M
Molecular and Functional Characterization of Chemerin ReceptorsR01AI079320 · NIAID · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI ZABEL, BRIAN A. · 2009 to 2013
$1.7M
Novel Dendritic Cell Chemoattractant and ReceptorR01AI059635 · NIAID · STANFORD UNIVERSITY · PI BUTCHER, EUGENE C · 2005 to 2009
$1.4M
SCOR in Cellular and Molecular Mechanisms of AsthmaP01HL067674 · NHLBI · STANFORD UNIVERSITY · PI GALLI, STEPHEN J · 2001 to 2001
$1.2M
ENDOTHELIAL CELL BIOLOGY IN INFLAMMATIONR01GM037734 · NIGMS · STANFORD UNIVERSITY · PI BUTCHER, EUGENE C · 1987 to 2017
$938k
Novel Dendritic Cell Chemoattractant and ReceptorR21AI059635 · NIAID · STANFORD UNIVERSITY · PI BUTCHER, EUGENE C · 2004 to 2004
$325k
CCR9 AND TECK IN INTESTINAL LYMPHOCYTE TRAFFICKINGR21AI047822 · NIAID · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI BUTCHER, EUGENE C · 2000 to 2000
$258k
NHLBI NIH HHS HL-67674NHLBI NIH HHS P01 HL067674NHLBI NIH HHS P50 HL067674NIAID NIH HHS AI-079320NIAID NIH HHS AI-47822NIAID NIH HHS AI-59635NIAID NIH HHS R01 AI047822NIAID NIH HHS R01 AI059635NIAID NIH HHS R01 AI079320NIAID NIH HHS R21 AI047822NIAID NIH HHS R21 AI059635NIAID NIH HHS R37 AI047822NIAID NIH HHS T32 AI007290NIGMS NIH HHS GM-37734NIGMS NIH HHS R01 GM037734NIGMS NIH HHS R37 GM037734
6 · The paper itself

Abstract

We examined the involvement of chemokine-like receptor-1 (CMKLR1) in experimental autoimmune encephalomyelitis (EAE), a model of human multiple sclerosis. Upon EAE induction by active immunization with myelin oligodendrocyte glycoprotein amino acids 35-55 (MOG(35-55)), microglial cells and CNS-infiltrating myeloid dendritic cells expressed CMKLR1, as determined by flow cytometric analysis. In addition, chemerin, a natural ligand for CMKLR1, was up-regulated in the CNS of mice with EAE. We found that CMKLR1-deficient (CMKLR1 knockout (KO)) mice develop less severe clinical and histologic disease than their wild-type (WT) counterparts. CMKLR1 KO lymphocytes proliferate and produce proinflammatory cytokines in vitro, yet MOG(35-55)-reactive CMKLR1 KO lymphocytes are deficient in their ability to induce EAE by adoptive transfer to WT or CMKLR1 KO recipients. Moreover, CMKLR1 KO recipients fail to fully support EAE induction by transferred MOG-reactive WT lymphocytes. The results imply involvement of CMKLR1 in both the induction and effector phases of disease. We conclude that CMKLR1 participates in the inflammatory mechanisms of EAE and represents a potential therapeutic target in multiple sclerosis.

Indexed as

Adoptive TransferAnimalsCentral Nervous SystemChemokinesChemotactic FactorsDendritic CellsEncephalomyelitis, Autoimmune, ExperimentalFemaleGlycoproteinsIntercellular Signaling Peptides and ProteinsInterferon-gammaInterleukin-17LeukocytesLipopolysaccharidesLymph NodesMacrophages, Peritonealchemerin protein, mouseChemokinesChemotactic FactorsCMKLR1 protein, mouseGlycoproteinsIntercellular Signaling Peptides and ProteinsInterferon-gammaInterleukin-17LipopolysaccharidesMyelin-Oligodendrocyte Glycoproteinmyelin oligodendrocyte glycoprotein (35-55)Peptide FragmentsReceptors, ChemokineReceptors, G-Protein-CoupledTumor Necrosis Factor-alpha

Identifiers

PMID19864606
PMCPMC2904075
OpenAlexW1923608016

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.