Evidence map›Paper›PMID 38633258›Full record

ArticleFrontiers in immunology2024

CD8

Jerome C Anyalebechi, Yini Sun, Carolyn Davis, Maylene E Wagener, Zhe Liang, Eileen M Burd, Craig M Coopersmith, Mandy L Ford

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2024. 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 31% 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, 3 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. 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

8 authors at 2 institutions in 2 countries.

Jerome C AnyalebechiDepartment of Surgery, Emory University School of Medicine, Atlanta, GA, United States.
Yini SunDepartment of Critical Care Medicine, The First Affiliated Hospital of China Medical University, China Medical University, Shenyang, China.
Carolyn DavisDepartment of Surgery, Emory University School of Medicine, Atlanta, GA, United States.
Maylene E WagenerDepartment of Surgery, Emory University School of Medicine, Atlanta, GA, United States.
Zhe LiangDepartment of Surgery, Emory University School of Medicine, Atlanta, GA, United States.
Eileen M BurdDepartment of Pathology and Laboratory Medicine, Emory University, Atlanta, GA, United States.
Craig M Coopersmith *Department of Surgery, Emory University School of Medicine, Atlanta, GA, United States.
Mandy L Ford *Department of Surgery, Emory University School of Medicine, Atlanta, GA, United States.
Emory University · USChina Medical University · CN

Funding

Critical Care Training ProgramT32GM095442 · NIGMS · EMORY UNIVERSITY · PI Craig M Coopersmith · 2011 to 2026
$4.7M
The Gut as a Target to Improve Outcomes in SepsisR35GM148217 · NIGMS · EMORY UNIVERSITY · PI Craig M Coopersmith · 2023 to 2026
$2.2M
Memory T Cell Cosigning Pathways in Sepsis-Induced Immune DysregulationR01AI149724 · NIAID · EMORY UNIVERSITY · PI FORD, MANDY L · 2020 to 2024
$1.9M
NIAID NIH HHS R01 AI149724NIGMS NIH HHS R35 GM148217NIGMS NIH HHS T32 GM095442
6 · The paper itself

Abstract

Introduction: A hallmark of T cell dysregulation during sepsis is the downregulation of costimulatory molecules. CD28 is one of T cell costimulatory molecules significantly altered on memory T cells during sepsis. We recently showed that treatment with a αCD28 agonist in septic immunologically experienced mice led to improved survival. Therefore, here we aimed to identify the cell subset(s) necessary for the survival benefit observed in the context of CD28 agonism, and to further investigate the mechanism by which CD28 agonism improves sepsis survival in immunologically experienced mice. Methods: Mice received specific pathogen inoculation to generate memory T cell populations similar in frequency to that of adult humans. Once these infections were cleared and the T cell response had transitioned to the memory phase, animals were rendered septic via cecal ligation and puncture in the presence or absence of an agonistic anti-CD28 mAb. Results: Results demonstrated that CD8 Discussion: Taken together, these results indicate that CD28 agonism in immunologically experienced mice effectively suppresses inflammation via a CD8

Indexed as

CD8-Positive T-LymphocytesSepsisAnimalsCD28 AntigensHumansMiceT-Lymphocytes, RegulatoryCD28 Antigenscostimulationmemory T cellregulatory T CellsepsisT lymhpocyte

Identifiers

PMID38633258
PMCPMC11021695
OpenAlexW4393867104

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.