Evidence map›Paper›PMID 38617240›Full record

ArticlebioRxiv : the preprint server for biology2024

High affinity chimeric antigen receptor signaling induces an inflammatory program in human regulatory T cells.

Russell W Cochrane, Rob A Robino, Bryan Granger, Eva Allen, Silvia Vaena, Martin J Romeo, Aguirre A de Cubas, Stefano Berto, Leonardo M R Ferreira

Open access · greenAbstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed, 5 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Russell W CochraneDepartment of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA.ORCID 0000-0003-2659-7987
Rob A RobinoDepartment of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA.ORCID 0000-0002-1645-0247
Bryan GrangerBioinformatics Core, Medical University of South Carolina, Charleston, SC, USA.ORCID 0009-0008-6663-3755
Eva AllenDepartment of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA.ORCID 0000-0002-6893-3582
Silvia VaenaHollings Cancer Center, Medical University of South Carolina, Charleston, SC, USA.
Martin J RomeoHollings Cancer Center, Medical University of South Carolina, Charleston, SC, USA.ORCID 0000-0001-7941-1862
Aguirre A de CubasDepartment of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA.ORCID 0000-0002-9185-9544
Stefano BertoBioinformatics Core, Medical University of South Carolina, Charleston, SC, USA.ORCID 0000-0001-9028-9458
Leonardo M R FerreiraDepartment of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA.ORCID 0000-0003-2491-9866
Medical University of South Carolina · US

Funding

Translational Science Laboratory Shared ResourceP30CA138313 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI Jian Ouyang · 2009 to 2026
$42.7M
Renewal of the Human Islet Research Enhancement Center (HIREC) for the Type-1-Diabetes-Focused Human Islet Research Network (HIRN).U24DK104162 · NIDDK · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI John S. Kaddis, Joyce Carol Niland · 2019 to 2026
$12.3M
Cellular, Biochemical and Molecular Sciences Training Program: Developing the skills and expertise needed for a changing biomedical landscapeT32GM132055 · NIGMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI Amy D Bradshaw, John P O'Bryan · 2019 to 2026
$3.9M
Activation of transposable elements as an endogenous source of neoepitopes and mediators of tumor immunogenicityK01CA245231 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI DE CUBAS, AGUIRRE A · 2020 to 2024
$600k
NCI NIH HHS K01 CA245231NCI NIH HHS P30 CA138313NIDDK NIH HHS U24 DK104162NIGMS NIH HHS T32 GM132055
6 · The paper itself

Abstract

Regulatory T cells (Tregs) are promising cellular therapies to induce immune tolerance in organ transplantation and autoimmune disease. The success of chimeric antigen receptor (CAR) T-cell therapy for cancer has sparked interest in using CARs to generate antigen-specific Tregs. Here, we compared CAR with endogenous T cell receptor (TCR)/CD28 activation in human Tregs. Strikingly, CAR Tregs displayed increased cytotoxicity and diminished suppression of antigen-presenting cells and effector T (Teff) cells compared with TCR/CD28 activated Tregs. RNA sequencing revealed that CAR Tregs activate Teff cell gene programs. Indeed, CAR Tregs secreted high levels of inflammatory cytokines, with a subset of FOXP3

Indexed as

Chimeric Antigen ReceptorHuman immunologyImmune cell therapyImmune toleranceInflammatory cytokinesReceptor affinityRegulatory T cellSynthetic immunologyT cell signaling

Identifiers

PMID38617240
PMCPMC11014479
OpenAlexW4393444602

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.