Evidence map›Paper›PMID 38073578›Full record

ArticleLife science alliance2024

A high-throughput two-cell assay for interrogating inhibitory signaling pathways in T cells.

Sumana Sharma, Toby Whitehead, Mateusz Kotowski, Emily Zhi Qing Ng, Joseph Clarke, Judith Leitner, Yi-Ling Chen, Ana Mafalda Santos, Peter Steinberger, Simon J Davis

Open access · goldAbstract read
In one paragraph

Article in Life science alliance, 2024. 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
0.2field-weighted citation impact, top 30% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  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

10 authors at 2 institutions in 2 countries.

Sumana SharmaMRC Translational Immune Discovery Unit, John Radcliffe Hospital, University of Oxford, Oxford, UK sumana.sharma@rdm.ox.ac.uk.ORCID https://orcid.org/0000-0003-0598-2181
Toby WhiteheadMRC Translational Immune Discovery Unit, John Radcliffe Hospital, University of Oxford, Oxford, UK.ORCID https://orcid.org/0009-0004-4528-6644
Mateusz KotowskiMRC Translational Immune Discovery Unit, John Radcliffe Hospital, University of Oxford, Oxford, UK.ORCID https://orcid.org/0000-0003-0236-0977
Emily Zhi Qing NgMRC Translational Immune Discovery Unit, John Radcliffe Hospital, University of Oxford, Oxford, UK.
Joseph ClarkeMRC Translational Immune Discovery Unit, John Radcliffe Hospital, University of Oxford, Oxford, UK.ORCID https://orcid.org/0009-0009-7631-4464
Judith LeitnerDivision of Immune Receptors and T Cell Activation, Institute of Immunology, Medical University of Vienna, Vienna, Austria.
Yi-Ling ChenMRC Translational Immune Discovery Unit, John Radcliffe Hospital, University of Oxford, Oxford, UK.ORCID https://orcid.org/0000-0003-3758-0638
Ana Mafalda SantosMRC Translational Immune Discovery Unit, John Radcliffe Hospital, University of Oxford, Oxford, UK.ORCID https://orcid.org/0000-0002-0015-5286
Peter SteinbergerDivision of Immune Receptors and T Cell Activation, Institute of Immunology, Medical University of Vienna, Vienna, Austria.
Simon J DavisMRC Translational Immune Discovery Unit, John Radcliffe Hospital, University of Oxford, Oxford, UK simon.davis@imm.ox.ac.uk.ORCID https://orcid.org/0000-0002-2280-1170
John Radcliffe Hospital · GBMedical University of Vienna · AT

Funding

Medical Research Council MR/Y015355/1Wellcome Trust
6 · The paper itself

Abstract

The recent success of immunotherapies relying on manipulation of T-cell activation highlights the value of characterising the mediators of immune checkpoint signaling. CRISPR/Cas9 is a popular approach for interrogating signaling pathways; however, the lack of appropriate assays for studying inhibitory signaling in T cells is limiting the use of large-scale perturbation-based approaches. Here, we adapted an existing Jurkat cell-based transcriptional reporter assay to study both activatory and inhibitory (PD-1-mediated) T-cell signaling using CRISPR-based genome screening in arrayed and pooled formats. We targeted 64 SH2 domain-containing proteins expressed by Jurkat T cells in an arrayed screen, in which individual targets could be assessed independently, showing that arrays can be used to study mediators of both activatory and inhibitory signaling. Pooled screens succeeded in simultaneously identifying many of the known mediators of proximal activating and inhibitory T-cell signaling, including SHP2 and PD-1, confirming the utility of the method. Altogether, the data suggested that SHP2 is the major PD-1-specific, SH2 family mediator of inhibitory signaling. These approaches should allow the systematic analysis of signaling pathways in T cells.

Indexed as

Programmed Cell Death 1 ReceptorT-LymphocytesHigh-Throughput Screening AssaysProteinsSignal TransductionProgrammed Cell Death 1 ReceptorProteins

Identifiers

PMID38073578
PMCPMC10703992
OpenAlexW4389431056

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.