Evidence map›Paper›PMID 25582188›Full record

ArticleAmerican journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons2015

Acute and chronic rejection: compartmentalization and kinetics of counterbalancing signals in cardiac transplants.

A M K Kaul, S Goparaju, N Dvorina, S Iida, K S Keslar, C A de la Motte, A Valujskikh, R L Fairchild, W M Baldwin

Open access · greenAbstract read
In one paragraph

Article in American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 33 citations in OpenAlex.

  1. Suppression of cardiac allograft vasculopathy by a macrophage efferocytosis receptor.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2026
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  18. Macrophage subpopulations and their impact on chronic allograft rejection versus graft acceptance in a mouse heart transplant model.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2018
    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

9 authors at 2 institutions in 1 country.

A M K KaulDepartment of Immunology, Cleveland Clinic, Cleveland, OH; Department of Biological, Geological, and Environmental Sciences, Cleveland State University, Cleveland, OH.
S Goparaju
N Dvorina
S Iida
K S Keslar
C A de la Motte
A Valujskikh
R L Fairchild
W M Baldwin
Cleveland Clinic · USCleveland State University · US

Funding

Surgery CoreP01AI087586 · NIAID · CLEVELAND CLINIC LERNER COM-CWRU · PI VALUJSKIKH, ANNA · 2010 to 2019
$17.2M
VERSICAN PROTEOLYSIS AND REGULATION OF VASCULAR SMOOTH MUSCLEP01HL107147 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI LAUER, MARK E · 2011 to 2017
$16.1M
NHLBI NIH HHS P01 HL107147NIAID NIH HHS 1P01 AI087586NIAID NIH HHS P01 AI087586
6 · The paper itself

Abstract

Acute and chronic rejection impact distinct compartments of cardiac allografts. Intramyocardial mononuclear cell infiltrates define acute rejection, whereas chronic rejection affects large arteries. Hearts transplanted from male to female C57BL/6 mice undergo acute rejection with interstitial infiltrates at 2 weeks that resolve by 6 weeks when large arteries develop arteriopathy. These processes are dependent on T cells because no infiltrates developed in T cell-deficient mice and transfer of CD4 T cells restored T cell as well as macrophage infiltrates and ultimately neointima formation. Markers of inflammatory macrophages were up-regulated in the interstitium acutely and decreased as markers of wound healing macrophages increased chronically. Programmed cell death protein, a negative costimulator, and its ligand PDL1 were up-regulated in the interstitium during resolution of acute rejection. Blocking PDL1:PD1 interactions in the acute phase increased interstitial T cell infiltrates. Toll-like receptor (TLR) 4 and its endogenous ligand hyaluronan were increased in arteries with neointimal expansion. Injection of hyaluronan fragments increased intragraft production of chemokines. Our data indicate that negative costimulatory pathways are critical for the resolution of acute interstitial infiltrates. In the arterial compartment recognition of endogenous ligands including hyaluronan by the innate TLRs may support the progression of arteriopathy.

Indexed as

Heart TransplantationAnimalsB7-H1 AntigenCD4-Positive T-LymphocytesChemokine CCL2Chemokine CXCL9FemaleGraft RejectionHyaluronic AcidMaleMiceMice, Inbred C57BLMice, KnockoutModels, AnimalMyocardiumSignal TransductionB7-H1 AntigenCcl2 protein, mouseCd274 protein, mouseChemokine CCL2Chemokine CXCL9Cxcl9 protein, mouseHyaluronic AcidTlr4 protein, mouseToll-Like Receptor 4Basic (laboratory) researchchemokine receptorschemokinesimmunobiologrejection: acuterejection: chronicscience

Identifiers

PMID25582188
PMCPMC4304877
OpenAlexW2112735926

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.