Evidence map›Paper›PMID 41366293›Full record

ArticleBMC immunology2025

T cell immunometabolic dysfunction in a mouse model of cecal ligation and puncture-induced sepsis.

Xiaoju Liu, Mai Liting, Peiyu Li, Zhong Chen, Zhijian Yu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC 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

5 authors.

Xiaoju LiuDepartment of Infectious Diseases, Shenzhen Key Laboratory for Endogenous Infections, Shenzhen Nanshan People's Hospital, Affiliated Nanshan Hospital of Shenzhen University, No 89 Taoyuan Road, Nanshan, Shenzhen, 518052, China.
Mai LitingDepartment of Pulmonary and Critical Care Medicine, the People's Hospital of Baoan Shenzhen, No. 118 Longjing 2nd Road, Xin'an Street, Bao'an, Shenzhen, 518100, China.
Peiyu LiDepartment of Infectious Diseases, Shenzhen Key Laboratory for Endogenous Infections, Shenzhen Nanshan People's Hospital, Affiliated Nanshan Hospital of Shenzhen University, No 89 Taoyuan Road, Nanshan, Shenzhen, 518052, China.
Zhong ChenDepartment of Infectious Diseases, Shenzhen Key Laboratory for Endogenous Infections, Shenzhen Nanshan People's Hospital, Affiliated Nanshan Hospital of Shenzhen University, No 89 Taoyuan Road, Nanshan, Shenzhen, 518052, China.
Zhijian YuDepartment of Infectious Diseases, Shenzhen Key Laboratory for Endogenous Infections, Shenzhen Nanshan People's Hospital, Affiliated Nanshan Hospital of Shenzhen University, No 89 Taoyuan Road, Nanshan, Shenzhen, 518052, China. yuzhijiansmu@163.com.

Funding

Medical Scientific Research Foundation of Guangdong Province, China B2023399Sanming Projectof Medicine in Shenzhen SZSM202303037the earmarked funding for Science, Technology and Innovation Commission of Shenzhen Municipality of basic research fund JCYJ20220530141810023the Shenzhen Nanshan District Scientific Research Program of the People's Republic of China NSZD2024001, NS2024001, NS2025031
6 · The paper itself

Abstract

backgroundT lymphocyte dysfunction is closely associated with immunosuppression in sepsis, whereas the underlying mechanisms are not fully understood.

resultsIn this study, we established a mouse model of cecal ligation and puncture (CLP)-induced sepsis and observed immunometabolic alterations in splenic T cells. Serum energy metabolites related to glycolysis and the tricarboxylic acid (TCA) cycle were imbalanced. Splenic T cells from septic mice showed a shift in subset distribution, with decreased naïve T cells and increased effector populations, along with concurrent activation and exhaustion phenotypes. Notably, mitochondrial mass and mitochondrial membrane potential were significantly diminished in both CD4

conclusionsOur findings provide several layers of T cell dysfunction in sepsis, linking subset redistribution, an exhausted phenotype, mitochondrial impairment, and reduced proliferative capacity, suggesting that future therapeutic interventions aiming to reverse sepsis-induced immunosuppression may require a combinatorial approach.

Indexed as

CD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCecumSepsisT-LymphocytesAnimalsAntigens, CDDisease Models, AnimalEnergy MetabolismGlycolysisHumansLigationLymphocyte ActivationMaleMembrane Potential, MitochondrialMiceAntigens, CDProgrammed Cell Death 1 ReceptorImmune metabolismMitochondrial massMitochondrial membrane potentialSepsisT cell

Identifiers

PMID41366293
PMCPMC12802186

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.