Evidence map›Paper›PMID 31085832›Full record

ArticleJCI insight2019

CCR4 expression on host T cells is a driver for alloreactive responses and lung rejection.

Vyacheslav Palchevskiy, Ying Ying Xue, Rita Kern, Stephen S Weigt, Aric L Gregson, Sophie X Song, Michael C Fishbein, Cory M Hogaboam, David M Sayah, Joseph P Lynch and 3 more

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

Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Platelets Independently Recruit into Asthmatic Lungs and Models of Allergic Inflammation via CCR3.American journal of respiratory cell and molecular biology · 2021
    Article
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

13 authors at 4 institutions in 3 countries.

Vyacheslav PalchevskiyDepartment of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Ying Ying XueDepartment of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Rita KernDepartment of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Stephen S WeigtDepartment of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Aric L GregsonDepartment of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Sophie X SongDepartment of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Michael C FishbeinDepartment of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Cory M HogaboamPulmonary & Critical Care Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
David M SayahDepartment of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Joseph P LynchDepartment of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Michael P KeaneUniversity College Dublin School of Medicine, Respiratory Medicine, St Vincent's University Hospital, Dublin, Ireland.
David G BrooksPrincess Margaret Cancer Center, University Health Network and Department of Immunology, University of Toronto, Toronto, Ontario, Canada.
John A BelperioDepartment of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
University of California, Los Angeles · USCedars-Sinai Medical Center · USPrincess Margaret Cancer Centre · CASt. Vincent's University Hospital · IE

Funding

Role of Surfactant Proteins in Mediating Noninfectious Inflammatory and FibroproP01HL108793 · NHLBI · DUKE UNIVERSITY · PI JIANG, DIANHUA · 2012 to 2022
$21.3M
Immune Mechanisms of AlloinjuryR01HL112990 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BELPERIO, JOHN A · 2012 to 2016
$2.2M
NHLBI NIH HHS P01 HL108793NHLBI NIH HHS R01 HL112990
6 · The paper itself

Abstract

Despite current immunosuppressive strategies, long-term lung transplant outcomes remain poor due to rapid allogenic responses. Using a stringent mouse model of allo-airway transplantation, we identify the CCR4-ligand axis as a central node driving secondary lymphoid tissue homing and activation of the allogeneic T cells that prevent long-term allograft survival. CCR4 deficiency on transplant recipient T cells diminishes allograft injury and when combined with CTLA4-Ig leads to an unprecedented long-term lung allograft accommodation. Thus, we identify CCR4-ligand interactions as a central mechanism driving allogeneic transplant rejection and suggest it as a potential target to enhance long-term lung transplant survival.

Indexed as

Adoptive TransferAllograftsAnimalsDisease Models, AnimalFemaleGraft RejectionGraft SurvivalHumansLungLung TransplantationMiceMice, KnockoutProof of Concept StudyReceptors, CCR4Signal TransductionT-LymphocytesCcr4 protein, mouseReceptors, CCR4Adaptive immunityChemokinesImmunologyT cellsTransplantation

Identifiers

PMID31085832
PMCPMC6629140
OpenAlexW2944979070

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.