Evidence map›Paper›PMID 32643825›Full record

ArticleThe EMBO journal2020

Rewired signaling network in T cells expressing the chimeric antigen receptor (CAR).

Rui Dong, Kendra A Libby, Franziska Blaeschke, Walker Fuchs, Alexander Marson, Ronald D Vale, Xiaolei Su

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
3.1field-weighted citation impact, top 6% 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

57 citing papers in PubMed, 71 citations in OpenAlex.

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  20. Converting TCR-based chimeric antigen receptor STAR into dual-specific targeting receptor for cancer immunotherapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
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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

7 authors at 4 institutions in 1 country.

Rui DongDepartment of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA, USA.ORCID 0000-0002-9118-3636
Kendra A LibbyDepartment of Cell Biology, Yale School of Medicine, New Haven, CT, USA.ORCID 0000-0003-2050-2940
Franziska BlaeschkeDepartment of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA, USA.
Walker FuchsDepartment of Cell Biology, Yale School of Medicine, New Haven, CT, USA.
Alexander MarsonDepartment of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA, USA.
Ronald D ValeDepartment of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA, USA.ORCID 0000-0003-3460-2758
Xiaolei SuDepartment of Cell Biology, Yale School of Medicine, New Haven, CT, USA.ORCID 0000-0001-8696-7922
University of California, San Francisco · USYale University · USHoward Hughes Medical Institute · USYale Cancer Center · US

Funding

American Cancer SocietyAndrew McDonough B+ FoundationBurroughs Wellcome FundCancer Research Institute (CRI)Care-for-Rare FoundationChan Zuckerberg BiohubCharles H. Hood FoundationGerman Research FoundationGilead SciencesHHS|National Institutes of Health (NIH)Howard Hughes Medical InstituteInnovative Genomics Institute (IGI)Jane Coffin Childs Memorial Fund for Medical Research (JCCF)Parker Institute for Cancer Immunotherapy (Parker Institute)Rally FoundationYale University (Yale)
6 · The paper itself

Abstract

The chimeric antigen receptor (CAR) directs T cells to target and kill specific cancer cells. Despite the success of CAR T therapy in clinics, the intracellular signaling pathways that lead to CAR T cell activation remain unclear. Using CD19 CAR as a model, we report that, similar to the endogenous T cell receptor (TCR), antigen engagement triggers the formation of CAR microclusters that transduce downstream signaling. However, CAR microclusters do not coalesce into a stable central supramolecular activation cluster (cSMAC). Moreover, LAT, an essential scaffold protein for TCR signaling, is not required for microcluster formation, immunological synapse formation, nor actin remodeling following CAR activation. However, CAR T cells still require LAT for an optimal production of the cytokine IL-2. Together, these data show that CAR T cells can bypass LAT for a subset of downstream signaling outputs, thus revealing a rewired signaling pathway as compared to native T cells.

Indexed as

HEK293 CellsHumansImmunological SynapsesInterleukin-2Jurkat CellsReceptors, Chimeric AntigenSignal TransductionT-LymphocytesIL2 protein, humanInterleukin-2Receptors, Chimeric AntigenactinCARimmunological synapseLATT cell signaling

Identifiers

PMID32643825
PMCPMC7429742
OpenAlexW3041575100

What OpenQuestion holds

Textmetadata
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.