Evidence map›Paper›PMID 38017505›Full record

ArticleJournal of translational medicine2023

C-C chemokine receptor 5 is essential for conventional NK cell trafficking and liver injury in a murine hepatitis virus-induced fulminant hepatic failure model.

Yun-Hui Liu, Lin Zhu, Zhong-Wei Zhang, Ting-Ting Liu, Qiu-Yu Cheng, Meng Zhang, Yu-Xin Niu, Lin Ding, Wei-Ming Yan, Xiao-Ping Luo and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 26% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. The Dual Role of Natural Killer Cells in the Septic Liver.Journal of inflammation research · 2026
    Review
  3. Article
  4. Review
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

12 authors at 3 institutions in 2 countries.

Yun-Hui Liu *Department of Infectious Diseases, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonostic Infectious Disease, Huazhong University of Science and Technology, 1095, Jiefang Avenue, Wuhan, 430030, People's Republic of China.
Lin Zhu *Department of Infectious Diseases, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonostic Infectious Disease, Huazhong University of Science and Technology, 1095, Jiefang Avenue, Wuhan, 430030, People's Republic of China.
Zhong-Wei ZhangDepartment of Infectious Diseases, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonostic Infectious Disease, Huazhong University of Science and Technology, 1095, Jiefang Avenue, Wuhan, 430030, People's Republic of China.
Ting-Ting LiuDepartment of Infectious Diseases, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonostic Infectious Disease, Huazhong University of Science and Technology, 1095, Jiefang Avenue, Wuhan, 430030, People's Republic of China.
Qiu-Yu ChengDepartment of Infectious Diseases, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonostic Infectious Disease, Huazhong University of Science and Technology, 1095, Jiefang Avenue, Wuhan, 430030, People's Republic of China.
Meng ZhangDepartment of Infectious Diseases, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonostic Infectious Disease, Huazhong University of Science and Technology, 1095, Jiefang Avenue, Wuhan, 430030, People's Republic of China.
Yu-Xin NiuDepartment of Infectious Diseases, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonostic Infectious Disease, Huazhong University of Science and Technology, 1095, Jiefang Avenue, Wuhan, 430030, People's Republic of China.
Lin DingDepartment of Infectious Diseases, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonostic Infectious Disease, Huazhong University of Science and Technology, 1095, Jiefang Avenue, Wuhan, 430030, People's Republic of China.
Wei-Ming YanDepartment of Infectious Diseases, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonostic Infectious Disease, Huazhong University of Science and Technology, 1095, Jiefang Avenue, Wuhan, 430030, People's Republic of China.
Xiao-Ping LuoDepartment of Pediatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095, Jiefang Avenue, Wuhan, 430030, Hubei Province, China.
Qin NingDepartment of Infectious Diseases, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonostic Infectious Disease, Huazhong University of Science and Technology, 1095, Jiefang Avenue, Wuhan, 430030, People's Republic of China. qning@vip.sina.com.
Tao ChenDepartment of Infectious Diseases, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonostic Infectious Disease, Huazhong University of Science and Technology, 1095, Jiefang Avenue, Wuhan, 430030, People's Republic of China. chentao_tjh@vip.sina.com.
Tongji Hospital · CNNational Public Health Laboratory · NPHuazhong University of Science and Technology · CN

Funding

National Key Research and Development Program of China 2021YFC2600200National Natural Science Foundation of China NO. 82170596Natural Science Foundation of Hubei Province 2021CFB353
6 · The paper itself

Abstract

backgroundPrevious studies have demonstrated that natural killer (NK) cells migrated into the liver from peripheral organs and exerted cytotoxic effects on hepatocytes in virus-induced liver failure.

aimThis study aimed to investigate the potential therapeutic role of chemokine receptors in the migration of NK cells in a murine hepatitis  virus strain 3 (MHV-3)-induced fulminant hepatic failure (MHV-3-FHF) model and its mechanism.

resultsBy gene array analysis, chemokine (C-C motif) receptor 5 (CCR5) was found to have remarkably elevated expression levels in hepatic NK cells after MHV-3 infection. The number of hepatic CCR5

conclusionThe CCR5-MIP-1β/RANTES axis played a critical role in the recruitment of cNK cells to the liver during MHV-3-induced liver injury. Targeted inhibition of CCR5 provides a therapeutic approach to ameliorate liver damage during virus-induced acute liver injury.

Indexed as

Liver Failure, AcuteMurine hepatitis virusAnimalsChemokine CCL3Chemokine CCL4Chemokine CCL5ChemokinesChemokines, CCKiller Cells, NaturalMiceReceptors, CCR5Receptors, ChemokineCCR5 protein, mouseChemokine CCL3Chemokine CCL4Chemokine CCL5ChemokinesChemokines, CCReceptors, CCR5Receptors, ChemokineCCR5ChemotaxisLiver failureNK cellVirus infection

Identifiers

PMID38017505
PMCPMC10685630
OpenAlexW4389151433

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.