Evidence map›Paper›PMID 25637591›Full record

ArticleJournal of leukocyte biology2015

Chemokine receptor CCR7 regulates the intestinal TH1/TH17/Treg balance during Crohn's-like murine ileitis.

Eóin N McNamee, Joanne C Masterson, Marisol Veny, Colm B Collins, Paul Jedlicka, Fergus R Byrne, Gordon Y Ng, Jesús Rivera-Nieves

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of leukocyte biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 12% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
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  12. Leukocyte Trafficking in Lymphatic Vessels.Cold Spring Harbor perspectives in medicine · 2022
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Eóin N McNamee*Mucosal Inflammation Program, School of Medicine, Gastrointestinal Eosinophilic Disease Program, Section of Pediatric Gastroenterology, Hepatology and Nutrition, Children's Hospital Colorado, and Department of Pathology, University of Colorado Denver, Colorado, USA; Department of Inflammation Research, Amgen, Thousand Oaks, California, USA; and Inflammatory Bowel Disease Center, Division of Gastroenterology, University of California San Diego and San Diego VA Medical Center, San Diego, California, USA eoin.mcnamee@ucdenver.edu.
Joanne C Masterson*Mucosal Inflammation Program, School of Medicine, Gastrointestinal Eosinophilic Disease Program, Section of Pediatric Gastroenterology, Hepatology and Nutrition, Children's Hospital Colorado, and Department of Pathology, University of Colorado Denver, Colorado, USA; Department of Inflammation Research, Amgen, Thousand Oaks, California, USA; and Inflammatory Bowel Disease Center, Division of Gastroenterology, University of California San Diego and San Diego VA Medical Center, San Diego, California, USA.
Marisol Veny*Mucosal Inflammation Program, School of Medicine, Gastrointestinal Eosinophilic Disease Program, Section of Pediatric Gastroenterology, Hepatology and Nutrition, Children's Hospital Colorado, and Department of Pathology, University of Colorado Denver, Colorado, USA; Department of Inflammation Research, Amgen, Thousand Oaks, California, USA; and Inflammatory Bowel Disease Center, Division of Gastroenterology, University of California San Diego and San Diego VA Medical Center, San Diego, California, USA.
Colm B Collins*Mucosal Inflammation Program, School of Medicine, Gastrointestinal Eosinophilic Disease Program, Section of Pediatric Gastroenterology, Hepatology and Nutrition, Children's Hospital Colorado, and Department of Pathology, University of Colorado Denver, Colorado, USA; Department of Inflammation Research, Amgen, Thousand Oaks, California, USA; and Inflammatory Bowel Disease Center, Division of Gastroenterology, University of California San Diego and San Diego VA Medical Center, San Diego, California, USA.
Paul Jedlicka*Mucosal Inflammation Program, School of Medicine, Gastrointestinal Eosinophilic Disease Program, Section of Pediatric Gastroenterology, Hepatology and Nutrition, Children's Hospital Colorado, and Department of Pathology, University of Colorado Denver, Colorado, USA; Department of Inflammation Research, Amgen, Thousand Oaks, California, USA; and Inflammatory Bowel Disease Center, Division of Gastroenterology, University of California San Diego and San Diego VA Medical Center, San Diego, California, USA.
Fergus R Byrne*Mucosal Inflammation Program, School of Medicine, Gastrointestinal Eosinophilic Disease Program, Section of Pediatric Gastroenterology, Hepatology and Nutrition, Children's Hospital Colorado, and Department of Pathology, University of Colorado Denver, Colorado, USA; Department of Inflammation Research, Amgen, Thousand Oaks, California, USA; and Inflammatory Bowel Disease Center, Division of Gastroenterology, University of California San Diego and San Diego VA Medical Center, San Diego, California, USA.
Gordon Y Ng*Mucosal Inflammation Program, School of Medicine, Gastrointestinal Eosinophilic Disease Program, Section of Pediatric Gastroenterology, Hepatology and Nutrition, Children's Hospital Colorado, and Department of Pathology, University of Colorado Denver, Colorado, USA; Department of Inflammation Research, Amgen, Thousand Oaks, California, USA; and Inflammatory Bowel Disease Center, Division of Gastroenterology, University of California San Diego and San Diego VA Medical Center, San Diego, California, USA.
Jesús Rivera-Nieves*Mucosal Inflammation Program, School of Medicine, Gastrointestinal Eosinophilic Disease Program, Section of Pediatric Gastroenterology, Hepatology and Nutrition, Children's Hospital Colorado, and Department of Pathology, University of Colorado Denver, Colorado, USA; Department of Inflammation Research, Amgen, Thousand Oaks, California, USA; and Inflammatory Bowel Disease Center, Division of Gastroenterology, University of California San Diego and San Diego VA Medical Center, San Diego, California, USA.
University of Colorado Denver · USAmgen (United States) · USUniversity of California San Diego Medical Center · US

Funding

Targeting L-Selectin in Chronic Murine IleitisR01DK080212 · NIDDK · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI RIVERA-NIEVES, JESUS · 2009 to 2013
$1.7M
Dendritic Cell Manipulation: A Novel Therapeutic for Inflammatory Bowel DiseaseI01BX001051 · VA · VA SAN DIEGO HEALTHCARE SYSTEM · PI RIVERA-NIEVES, JESUS · 2011 to 2015
–
BLRD VA I01 BX001051NIDDK NIH HHS DK080212NIDDK NIH HHS R01 DK080212
6 · The paper itself

Abstract

The regulation of T cell and DC retention and lymphatic egress within and from the intestine is critical for intestinal immunosurveillance; however, the cellular processes that orchestrate this balance during IBD remain poorly defined. With the use of a mouse model of TNF-driven Crohn's-like ileitis (TNF(Δ) (ARE)), we examined the role of CCR7 in the control of intestinal T cell and DC retention/egress during experimental CD. We observed that the frequency of CCR7-expressing TH1/TH17 effector lymphocytes increased during active disease in TNF(Δ) (ARE) mice and that ΔARE/CCR7(-/-) mice developed exacerbated ileitis and multiorgan inflammation, with a marked polarization and ileal retention of TH1 effector CD4(+) T cells. Furthermore, adoptive transfer of ΔARE/CCR7(-/-) effector CD4(+) into lymphopenic hosts resulted in ileo-colitis, whereas those transferred with ΔARE/CCR7(+/+) CD4(+) T cells developed ileitis. ΔARE/CCR7(-/-) mice had an acellular draining MLN, decreased CD103(+) DC, and decreased expression of RALDH enzymes and of CD4(+)CD25(+)FoxP3(+) Tregs. Lastly, a mAb against CCR7 exacerbated ileitis in TNF(Δ) (ARE) mice, phenocopying the effects of congenital CCR7 deficiency. Our data underscore a critical role for the lymphoid chemokine receptor CCR7 in orchestrating immune cell traffic and TH1 versus TH17 bias during chronic murine ileitis.

Indexed as

Adoptive TransferAldehyde DehydrogenaseAnimalsAntibodies, MonoclonalAntigens, CDCell MovementCrohn DiseaseDendritic CellsDisease Models, AnimalGene Expression RegulationHumansIleitisIleumIsoenzymesMiceMice, TransgenicAldehyde DehydrogenaseAntibodies, MonoclonalAntigens, CDCcr7 protein, mouseIsoenzymesReceptors, CCR7Tumor Necrosis Factor-alphaCD103+ dendritic cellsCrohn’s diseaseeffector memory T cellsinflammatory bowel diseaselymphatics

Identifiers

PMID25637591
PMCPMC4438744
OpenAlexW1966345872

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.