Evidence map›Paper›PMID 36867228›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2023

Blocking of programmed cell death-ligand 1 (PD-L1) expressed on endothelial cells promoted the recruitment of CD8

Qi Li, Simeng Wei, Yue Li, Fengjiao Wu, Xiaoling Qin, Zhongsha Li, Jingyu Li, Chang Chen

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. CD8Nature reviews. Cardiology · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Review
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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

8 authors at 2 institutions in 1 country.

Qi LiThe Biotherapy Center, Tumor Hospital of Harbin Medical University, 150 Haping Road, Harbin, People's Republic of China.
Simeng WeiDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Baojian Road 157, Harbin, 150086, Heilongjiang, People's Republic of China.
Yue LiDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Baojian Road 157, Harbin, 150086, Heilongjiang, People's Republic of China.
Fengjiao WuThe Biotherapy Center, Tumor Hospital of Harbin Medical University, 150 Haping Road, Harbin, People's Republic of China.
Xiaoling QinThe Biotherapy Center, Tumor Hospital of Harbin Medical University, 150 Haping Road, Harbin, People's Republic of China.
Zhongsha LiDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Baojian Road 157, Harbin, 150086, Heilongjiang, People's Republic of China.
Jingyu LiDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Baojian Road 157, Harbin, 150086, Heilongjiang, People's Republic of China.
Chang ChenDepartment of Pharmacology (State-Province Key Laboratories of Biomedicine Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Baojian Road 157, Harbin, 150086, Heilongjiang, People's Republic of China. chen213chang@163.com.
Harbin Medical University · CNThird Affiliated Hospital of Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProgrammed death ligand-1 (PD-L1) is involved in the negative regulation of immune responses in a variety of diseases. We evaluated the contribution of PD-L1 to the activation of immune cells that promote atherosclerotic lesion formation and inflammation. METHODS AND

resultsCompared to ApoE

conclusionsOur findings highlighted that blocking of PD-L1 promoted up-regulation of CD8 + IFN-γ + T cell-mediated immune responses, leading to the secretion of inflammatory cytokine that exacerbated the atherosclerotic burden and promoted inflammation. However, further studies are needed to gain insight into whether PD-L1 activation could be a novel immunotherapy strategy for atherosclerosis.

Indexed as

AtherosclerosisCD8-Positive T-LymphocytesAnimalsApoptosisCholesterolCytokinesEndothelial CellsInflammationInterferon-gammaLigandsMiceProgrammed Cell Death 1 ReceptorCholesterolCytokinesInterferon-gammaLigandsProgrammed Cell Death 1 ReceptorAtherosclerosisCD8+IFN-γ+T cellEndothelial cellIFN-γPD-L1

Identifiers

PMID36867228
OpenAlexW4323035216

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.