Evidence map›Paper›PMID 37796477›Full record

ArticleThe Journal of experimental medicine2023

TCR ligand potency differentially impacts PD-1 inhibitory effects on diverse signaling pathways.

Waipan Chan, Yuqi M Cao, Xiang Zhao, Edward C Schrom, Dongya Jia, Jian Song, Leah V Sibener, Shen Dong, Ricardo A Fernandes, Clinton J Bradfield and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
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  15. CD8Journal of translational medicine · 2024
    Review
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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

16 authors at 4 institutions in 1 country.

Waipan ChanLymphocyte Biology Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0002-9109-6583
Yuqi M CaoLymphocyte Biology Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID 0009-0002-1757-2649
Xiang ZhaoDepartment of Molecular and Cellular Physiology and Structural Biology, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0002-0043-324X
Edward C SchromLymphocyte Biology Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0002-1793-6433
Dongya JiaImmunodynamics Group, Laboratory of Integrative Cancer Immunology, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.ORCID 0000-0002-6307-8580
Jian SongLymphocyte Biology Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0002-0289-3063
Leah V SibenerDepartment of Molecular and Cellular Physiology and Structural Biology, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0001-9737-8517
Shen DongDepartment of Molecular and Cellular Physiology and Structural Biology, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0001-8839-7046
Ricardo A FernandesDepartment of Molecular and Cellular Physiology and Structural Biology, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0001-5343-3334
Clinton J BradfieldSignaling Systems Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0001-6410-3517
Margery SmelkinsonBiological Imaging Section, Research Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0001-7777-5574
Juraj KabatBiological Imaging Section, Research Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0001-8636-542X
Jyh Liang HorLymphocyte Biology Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0001-6721-4204
Grégoire Altan-BonnetImmunodynamics Group, Laboratory of Integrative Cancer Immunology, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.ORCID 0000-0002-7283-3162
K Christopher GarciaDepartment of Molecular and Cellular Physiology and Structural Biology, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0001-9273-0278
Ronald N GermainLymphocyte Biology Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0003-1495-9143
National Institutes of Health · USStanford University · USNational Cancer Institute · USHoward Hughes Medical Institute · US

Funding

Structural correlates of T cell receptor signalingR01AI103867 · NIAID · STANFORD UNIVERSITY · PI Kenan Christopher GARCIA · 2014 to 2026
$5.3M
Strategies for Receptor inhibition in immunotherapyR01CA177684 · NCI · STANFORD UNIVERSITY · PI DOUGAN, MICHAEL LAWRENCE, GARCIA, KENAN CHRISTOPHER · 2014 to 2025
$3.5M
Howard Hughes Medical InstituteNCI NIH HHS R01 CA177684NIAID NIH HHS R01 AI103867NIH HHS 5R01AI103867
6 · The paper itself

Abstract

Checkpoint blockade revolutionized cancer therapy, but we still lack a quantitative, mechanistic understanding of how inhibitory receptors affect diverse signaling pathways. To address this issue, we developed and applied a fluorescent intracellular live multiplex signal transduction activity reporter (FILMSTAR) system to analyze PD-1-induced suppressive effects. These studies identified pathways triggered solely by TCR or requiring both TCR and CD28 inputs. Using presenting cells differing in PD-L1 and CD80 expression while displaying TCR ligands of distinct potency, we found that PD-1-mediated inhibition primarily targets TCR-linked signals in a manner highly sensitive to peptide ligand quality. These findings help resolve discrepancies in existing data about the site(s) of PD-1 inhibition in T cells while emphasizing the importance of neoantigen potency in controlling the effects of checkpoint therapy.

Indexed as

Programmed Cell Death 1 ReceptorSignal TransductionB7-H1 AntigenLigandsReceptors, Antigen, T-CellT-LymphocytesB7-H1 AntigenLigandsProgrammed Cell Death 1 ReceptorReceptors, Antigen, T-Cell

Identifiers

PMID37796477
PMCPMC10555889
OpenAlexW4387356898

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.