Evidence map›Paper›PMID 40510337›Full record

ArticleFrontiers in immunology2025

DOCK2 protects against bacterial sepsis by constraining T helper 1 response.

Shusen Ye, Linzi Huang, Yuhao Zheng, Shanshan Liu, Xiangyang Wang, Haoyuan Yu, Lisi Zhu, Texi Liang, Yifei Wang, Chunmin Zhang and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

13 authors.

Shusen Ye *Guangdong Provincial Key Laboratory of Immune Regulation and Immunotherapy, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, China.
Linzi Huang *Guangdong Provincial Key Laboratory of Immune Regulation and Immunotherapy, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, China.
Yuhao Zheng *Guangdong Provincial Key Laboratory of Immune Regulation and Immunotherapy, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, China.
Shanshan Liu *Guangdong Provincial Key Laboratory of Immune Regulation and Immunotherapy, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, China.
Xiangyang WangGuangdong Cardiovascular Institute, Guangdong, Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
Haoyuan YuDepartment of Hepatic Surgery and Liver Transplantation Center, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Lisi ZhuGuangdong Provincial Key Laboratory of Immune Regulation and Immunotherapy, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, China.
Texi LiangGuangdong Provincial Key Laboratory of Immune Regulation and Immunotherapy, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, China.
Yifei WangInstitute of Immunological Innovation and Translation, Institute of Life Sciences, Chongqing Medical University, Chongqing, China.
Chunmin ZhangPediatric Intensive Care Unit, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Fan WuDepartment of Neonatology, Guangzhou Key Laboratory of Neonatal Intestinal Diseases, the Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Lilin YeGuangdong Provincial Key Laboratory of Immune Regulation and Immunotherapy, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, China.
Yingjiao CaoGuangdong Provincial Key Laboratory of Immune Regulation and Immunotherapy, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Sepsis is a systemic host response to infection with life-threatening consequence which ranks among the top ten causes of death worldwide. Nevertheless, our understanding of the molecular and cellular impact of sepsis remains rudimentary. Methods: A mouse sepsis model was established through LPS induction and Results: We identified dedicator of cytokinesis 2 (DOCK2) is a critical downregulating factor for LPS signal pathways. DOCK2-deficient mice were highly sensitive to LPS-induced sepsis and Conclusion: Our data indicates that DOCK2 acts as a protective role in regulating systemic inflammation and multi-organ injury in bacterial sepsis by constraining Th1 response. These findings provide new targets for immunomodulatory therapy of sepsis, suggesting that targeting the DOCK2-Th1 axis may become a new strategy to improve systemic inflammatory responses associated with bacterial infections.

Indexed as

Escherichia coliEscherichia coli InfectionsGTPase-Activating ProteinsSepsisTh1 CellsAnimalsCytokinesDisease Models, AnimalGuanine Nucleotide Exchange FactorsInterferon-gammaLipopolysaccharidesMiceMice, Inbred C57BLMice, KnockoutSignal TransductionCytokinesDOCK2 protein, mouseGTPase-Activating ProteinsGuanine Nucleotide Exchange FactorsInterferon-gammaLipopolysaccharidesDOCK2E.coliLPSsepsisTh1

Identifiers

PMID40510337
PMCPMC12158923

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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.