Evidence map›Paper›PMID 35983991›Full record

ArticleeLife2022

HLJ1 amplifies endotoxin-induced sepsis severity by promoting IL-12 heterodimerization in macrophages.

Wei-Jia Luo, Sung-Liang Yu, Chia-Ching Chang, Min-Hui Chien, Ya-Ling Chang, Keng-Mao Liao, Pei-Chun Lin, Kuei-Pin Chung, Ya-Hui Chuang, Jeremy J W Chen and 2 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

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  8. Inflammatory factors collaboratively linkFrontiers in immunology · 2025
    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

12 authors at 3 institutions in 2 countries.

Wei-Jia LuoDepartment of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Sung-Liang YuDepartment of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Chia-Ching ChangDepartment of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Min-Hui ChienDepartment of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Ya-Ling ChangDepartment of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Keng-Mao LiaoGenome and Systems Biology Degree Program, National Taiwan University and Academia Sinica, Taipei, Taiwan.
Pei-Chun LinDepartment of Laboratory Medicine, National Taiwan University, Taipei, Taiwan.
Kuei-Pin ChungDepartment of Laboratory Medicine, National Taiwan University, Taipei, Taiwan.
Ya-Hui ChuangDepartment of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Jeremy J W ChenInstitute of Biomedical Sciences, National Chung Hsing University, Taichung, Taiwan.
Pan-Chyr YangDepartment of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Kang-Yi SuDepartment of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, Taipei, Taiwan.ORCID 0000-0002-6538-9526
National Taiwan University · TWInstitute of Biomedical Sciences, Academia Sinica · TWNational Chung Hsing University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heat shock protein (HSP) 40 has emerged as a key factor in both innate and adaptive immunity, whereas the role of HLJ1, a molecular chaperone in HSP40 family, in modulating endotoxin-induced sepsis severity is still unclear. During lipopolysaccharide (LPS)-induced endotoxic shock, HLJ1 knockout mice shows reduced organ injury and IFN-γ (interferon-γ)-dependent mortality. Using single-cell RNA sequencing, we characterize mouse liver nonparenchymal cell populations under LPS stimulation, and show that HLJ1 deletion affected IFN-γ-related gene signatures in distinct immune cell clusters. In CLP models, HLJ1 deletion reduces IFN-γ expression and sepsis mortality rate when mice are treated with antibiotics. HLJ1 deficiency also leads to reduced serum levels of IL-12 in LPS-treated mice, contributing to dampened production of IFN-γ in natural killer cells but not CD4

Indexed as

Interleukin-12SepsisAnimalsCD8-Positive T-LymphocytesEndotoxinsHSP40 Heat-Shock ProteinsInterferon-gammaLipopolysaccharidesMacrophagesMiceMice, KnockoutEndotoxinsHSP40 Heat-Shock ProteinsInterferon-gammaInterleukin-12Lipopolysaccharidescell biologyDNAJB4HLJ1IFN-γIL-12immunologyinflammationlipopolysaccharidemousesepsis

Identifiers

PMID35983991
PMCPMC9457701
OpenAlexW4294992208

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.