Evidence map›Paper›PMID 38327049›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2024

Mechanical force determines chimeric antigen receptor microclustering and signaling.

Yue Qiu, Qingyue Xiao, Yucai Wang, Yichen Cao, Jing Wang, Zhengpeng Wan, Xiangjun Chen, Wanli Liu, Li Ma, Chenguang Xu

Open access · bronzeAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

7 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Small-molecule control of CAR T cells.Nature reviews. Chemistry · 2025
    Review
  5. Review
  6. Article
  7. Review
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 5 institutions in 2 countries.

Yue QiuInstitute of Molecular Immunology, Department of Biotechnology, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou 510515, China.
Qingyue XiaoInstitute of Molecular Immunology, Department of Biotechnology, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou 510515, China.
Yucai WangInstitute of Molecular Immunology, Department of Biotechnology, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou 510515, China.
Yichen CaoInstitute of Molecular Immunology, Department of Biotechnology, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou 510515, China.
Jing WangDepartment of Biological Sciences, Virginia Tech, Blacksburg, VA 24061, USA.
Zhengpeng WanDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Xiangjun ChenCenter for Infectious Disease Research, School of Medicine, Westlake University, Hangzhou 310024, China; School of Life Sciences, Westlake University, Hangzhou 310024, China.
Wanli LiuMOE Key Laboratory of Protein Sciences, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, School of Life Sciences, Tsinghua University, Beijing 100084, China; Tsinghua-Peking Center for Life Sciences, Beijing 100084, China.
Li MaInstitute of Molecular Immunology, Department of Biotechnology, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou 510515, China. Electronic address: mali_61648322@smu.edu.cn.
Chenguang XuInstitute of Molecular Immunology, Department of Biotechnology, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou 510515, China. Electronic address: xuchenguang@smu.edu.cn.
Southern Medical University · CNCenter for Life Sciences · CNMassachusetts Institute of Technology · USVirginia Tech · USWestlake University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chimeric antigen receptor (CAR) T cells are activated to trigger the lytic machinery after antigen engagement, and this has been successfully applied clinically as therapy. The mechanism by which antigen binding leads to the initiation of CAR signaling remains poorly understood. Here, we used a set of short double-stranded DNA (dsDNA) tethers with mechanical forces ranging from ∼12 to ∼51 pN to manipulate the mechanical force of antigen tether and decouple the microclustering and signaling events. Our results revealed that antigen-binding-induced CAR microclustering and signaling are mechanical force dependent. Additionally, the mechanical force delivered to the antigen tether by the CAR for microclustering is generated by autonomous cell contractility. Mechanistically, the mechanical-force-induced strong adhesion and CAR diffusion confinement led to CAR microclustering. Moreover, cytotoxicity may have a lower mechanical force threshold than cytokine generation. Collectively, these results support a model of mechanical-force-induced CAR microclustering for signaling.

Indexed as

Receptors, Chimeric AntigenAntigensImmunotherapy, AdoptiveReceptors, Antigen, T-CellSignal TransductionAntigensReceptors, Antigen, T-CellReceptors, Chimeric AntigenCARdsDNA tethermechanical forcemicroclusteringsignaling

Identifiers

PMID38327049
PMCPMC11163199
OpenAlexW4391578116

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.