Evidence map›Paper›PMID 28738836›Full record

ReviewJournal of hematology & oncology2017

Metabolism-associated danger signal-induced immune response and reverse immune checkpoint-activated CD40

Jin Dai, Pu Fang, Jason Saredy, Hang Xi, Cueto Ramon, William Yang, Eric T Choi, Yong Ji, Wei Mao, Xiaofeng Yang and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in Journal of hematology & oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

27 citing papers in PubMed, 41 citations in OpenAlex.

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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

11 authors at 3 institutions in 2 countries.

Jin DaiDepartment of Cardiology, The First Affiliated Hospital of Zhejiang Chinese Medical University, 54 Youdian road, Hangzhou, 310006, Zhejiang, China.
Pu FangCenter for Metabolic Disease Research, Temple University School of Medicine, 3500 N. Broad Street, Philadelphia, PA, 19140, USA.
Jason SaredyCenter for Metabolic Disease Research, Temple University School of Medicine, 3500 N. Broad Street, Philadelphia, PA, 19140, USA.
Hang XiCenter for Metabolic Disease Research, Temple University School of Medicine, 3500 N. Broad Street, Philadelphia, PA, 19140, USA.
Cueto RamonCenter for Metabolic Disease Research, Temple University School of Medicine, 3500 N. Broad Street, Philadelphia, PA, 19140, USA.
William YangCenter for Metabolic Disease Research, Temple University School of Medicine, 3500 N. Broad Street, Philadelphia, PA, 19140, USA.
Eric T ChoiDepartment of Surgery, Temple University School of Medicine, 3500 N. Broad Street, Philadelphia, PA, 19140, USA.
Yong JiKey Laboratory of Cardiovascular and Cerebrovascular Medicine, School of Pharmacy, Nanjing Medical University, Nanjing, 210029, China.
Wei MaoDepartment of Cardiology, The First Affiliated Hospital of Zhejiang Chinese Medical University, 54 Youdian road, Hangzhou, 310006, Zhejiang, China. maoweilw@163.com.
Xiaofeng YangCenter for Metabolic Disease Research, Temple University School of Medicine, 3500 N. Broad Street, Philadelphia, PA, 19140, USA.
Hong WangCenter for Metabolic Disease Research, Temple University School of Medicine, 3500 N. Broad Street, Philadelphia, PA, 19140, USA. hongw@temple.edu.
Temple University · USNanjing Medical University · CNZhejiang Chinese Medical University · CN

Funding

CD40 monocyte in chronic kidney diseaseR01DK113775 · NIDDK · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2017 to 2021
$3.3M
Hyperhomocysteinemia and HDL MetabolismR01HL117654 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2013 to 2017
$3.0M
Caspase-1 activation mediates chronic kidney disease-accelerated atherosclerosisR01HL131460 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI CHOI, ERIC T., WANG, HONG · 2016 to 2019
$2.8M
The roles of miR-155 in regulating atherosclerosis and metabolically healthy obesityR01HL138749 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI YANG, XIAOFENG · 2017 to 2020
$2.6M
NADHP Oxidase-mediated MC differentiation & Endothelial Dysfunction in HHcyR01HL110764 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2011 to 2015
$2.5M
Atherogenic roles of complement systemR01HL130233 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI QIN, XUEBIN, WANG, HONG · 2016 to 2019
$2.5M
IL-35 suppression of endothelial cell activation and atherosclerosisR01HL132399 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI YANG, XIAOFENG · 2017 to 2020
$2.3M
HHcy-induced Inflammatory Monocyte and Macrophage Differentiation in DiabetesR01DK104116 · NIDDK · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2015 to 2019
$2.2M
Roles of Interleukin-17 in Endothelial CellsR01HL108910 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI YANG, XIAOFENG · 2011 to 2015
$1.9M
Role of HHcy in diabetic vascular diseaseR01HL082774 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2006 to 2010
$1.8M
HHcy-induced Bax upregulation, Treg apoptosis and vascular diseaseR01HL116917 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI YANG, XIAOFENG · 2013 to 2016
$1.6M
PRECONDITIONING MECHANISMS REGULATING ISCHEMIAF32HL009445 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI MELDRUM, DANIEL R · 1996 to 1997
–
NHLBI NIH HHS F32 HL009445NHLBI NIH HHS R01 HL082774NHLBI NIH HHS R01 HL108910NHLBI NIH HHS R01 HL110764NHLBI NIH HHS R01 HL116917NHLBI NIH HHS R01 HL117654NHLBI NIH HHS R01 HL130233NHLBI NIH HHS R01 HL131460NHLBI NIH HHS R01 HL132399NHLBI NIH HHS R01 HL138749NIDDK NIH HHS R01 DK104116NIDDK NIH HHS R01 DK113775
6 · The paper itself

Abstract

Adaptive immunity is critical for disease progression and modulates T cell (TC) and antigen-presenting cell (APC) functions. Three signals were initially proposed for adaptive immune activation: signal 1 antigen recognition, signal 2 co-stimulation or co-inhibition, and signal 3 cytokine stimulation. In this article, we propose to term signal 2 as an immune checkpoint, which describes interactions of paired molecules leading to stimulation (stimulatory immune checkpoint) or inhibition (inhibitory immune checkpoint) of an immune response. We classify immune checkpoint into two categories: one-way immune checkpoint for forward signaling towards TC only, and two-way immune checkpoint for both forward and reverse signaling towards TC and APC, respectively. Recently, we and others provided evidence suggesting that metabolic risk factors (RF) activate innate and adaptive immunity, involving the induction of immune checkpoint molecules. We summarize these findings and suggest a novel theory, metabolism-associated danger signal (MADS) recognition, by which metabolic RF activate innate and adaptive immunity. We emphasize that MADS activates the reverse immune checkpoint which leads to APC inflammation in innate and adaptive immunity. Our recent evidence is shown that metabolic RF, such as uremic toxin or hyperhomocysteinemia, induced immune checkpoint molecule CD40 expression in monocytes (MC) and elevated serum soluble CD40 ligand (sCD40L) resulting in CD40

Indexed as

CD40 AntigensCell DifferentiationHumansLymphocyte ActivationMonocytesSignal TransductionCD40 AntigensCD40+ MCImmune checkpointMetabolic risk factorsMetabolism-associated danger signalReverse-immune checkpoint

Identifiers

PMID28738836
PMCPMC5525309
OpenAlexW2738626014

What OpenQuestion holds

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Registered trials

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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.