Evidence map›Paper›PMID 27618275›Full record

ArticleCritical care medicine2017

Suppression of T Cell Autophagy Results in Decreased Viability and Function of T Cells Through Accelerated Apoptosis in a Murine Sepsis Model.

Takehiko Oami, Eizo Watanabe, Masahiko Hatano, Satoshi Sunahara, Lisa Fujimura, Akemi Sakamoto, Chizuru Ito, Kiyotaka Toshimori, Shigeto Oda

Registry-linked trialOpen access · hybridAbstract read
In one paragraph

Article in Critical care medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05524376 (Regulatory Network and Diagnostic Value of Key Autophagy-related Genes in Sepsis), which is not on this map. Cited by 59 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 2 pooled it
6.0field-weighted citation impact, top 3% 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.

NCT05524376 unknown statusnot on this mapstarted 2022, after this paper: background citation

Regulatory Network and Diagnostic Value of Key Autophagy-related Genes in Sepsis

TypeobservationalSponsorSun Yat-Sen Memorial Hospital of Sun Yat-Sen UniversityRan2022 to 2022Enrolled40ConditionsSepsis, AutophagyArmsno intervention
3 · Its place in the literature

Who cites it

59 citing papers in PubMed, 2 syntheses or guidelines pooled it, 86 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. The Role of Vitamin D and Vitamin D Receptor in Sepsis.Current issues in molecular biology · 2025
    Review
  10. Article
  11. Review
  12. Lymphopenia in sepsis: a narrative review.Critical care (London, England) · 2024
    Review
  13. Observational
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Takehiko Oami1Department of Emergency and Critical Care Medicine, Chiba University Graduate School of Medicine, Chiba, Japan. 2Department of Biomedical Science, Graduate School of Medicine, Chiba University, Chiba, Japan. 3Department of Reproductive Biology and Medicine, Chiba University Graduate School of Medicine, Chiba, Japan.
Eizo Watanabe
Masahiko Hatano
Satoshi Sunahara
Lisa Fujimura
Akemi Sakamoto
Chizuru Ito
Kiyotaka Toshimori
Shigeto Oda
Chiba University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveWhile type 1 programmed cell death (apoptosis) of T cells leads to immunosuppression in sepsis, a crosstalk between apoptosis and autophagy (type 2 programmed cell death) has not been shown. The aim of this study is to elucidate the details of the interaction between autophagy and immunosuppression.

designLaboratory investigation in the murine sepsis model.

settingUniversity laboratory. SUBJECTS: Six- to 8-week-old male mice.

interventionsWe investigated the kinetics of autophagy in T cells from spleen in a cecal ligation and puncture model with green fluorescent protein-microtubule-associated protein light chain 3 transgenic mice. We analyzed apoptosis, mitochondrial homeostasis and cytokine production in T cells, and survival rate after cecal ligation and puncture using T cell-specific autophagy-deficient mice. MEASUREMENTS AND MAIN

resultsWe observed an increase of autophagosomes, which was assessed by flow cytometry. However, an autophagy process in CD4 T cells during sepsis was insufficient including the accumulation of p62. On the other hand, a blockade of autophagy accelerated T cell apoptosis compared with the control mice, augmenting the gene expression of Bcl-2-like 11 and programmed cell death 1. Furthermore, mitochondrial accumulation in T cells occurred via a blockade of autophagy during sepsis. In addition, interleukin-10 production in CD4 T cells from the cecal ligation and puncture-operated knockout mice was markedly increased. Consequently, deficiency of autophagy in T cells significantly decreased the survival rate in the murine sepsis model.

conclusionsWe demonstrated that blocking autophagy accelerated apoptosis and increased mortality in concordance with the insufficient autophagy process in CD4 T cells in the murine sepsis model, suggesting that T cell autophagy plays a protective role against apoptosis and immunosuppression in sepsis.

Indexed as

ApoptosisAnimalsAutophagyB7-H1 AntigenBcl-2-Like Protein 11CecumCell SurvivalDisease Models, AnimalInterleukin-10MaleMice, KnockoutMice, TransgenicMitochondriaSepsisSpleenT-LymphocytesB7-H1 AntigenBcl-2-Like Protein 11Cd274 protein, mouseInterleukin-10

Identifiers

PMID27618275
PMCPMC5364514
OpenAlexW2513248675

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Registered trials

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.