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Related Concept Videos

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Updated: Jul 11, 2025

In Vivo Immunogenicity Screening of Tumor-Derived Extracellular Vesicles by Flow Cytometry of Splenic T Cells
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Esophageal cancer cell-derived small extracellular vesicles decrease circulating Tfh/Tfr via sEV-PDL1 to promote

Zijie Li1, Yuehua Zhang2, He Hao3

  • 1Hebei Medical University, Shijiazhuang, 050011, Hebei, China.

Cancer Immunology, Immunotherapy : CII
|November 9, 2023
PubMed
Summary
This summary is machine-generated.

Small extracellular vesicles expressing PD-L1 (sEV-PDL1) in esophageal cancer (EC) disrupt Tfh/Tfr cell balance, promoting immune escape. Targeting sEV-PDL1 may restore this balance and offer a new EC therapy.

Keywords:
Esophageal cancerFollicular helper T cellsFollicular regulatory T cellsImmunosuppressionsEV-PDL1

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Area of Science:

  • Immunology
  • Oncology
  • Extracellular Vesicles Research

Background:

  • Esophageal cancer (EC) progression is linked to immune evasion.
  • Small extracellular vesicles (sEVs) expressing programmed death ligand 1 (sEV-PDL1) contribute to tumor immune escape.
  • An imbalance between circulating follicular helper T (Tfh) and follicular regulatory T (Tfr) cells is implicated in various cancers.

Purpose of the Study:

  • To investigate the role of EC-derived sEV-PDL1 in regulating circulating Tfh and Tfr cells.
  • To elucidate the mechanism by which sEV-PDL1 influences Tfh/Tfr cell balance and function.
  • To explore the therapeutic potential of targeting sEV-PDL1 in EC.

Main Methods:

  • Flow cytometry to detect circulating Tfh and Tfr cells in EC patients and healthy donors (HDs).
  • Isolation and characterization of sEVs from EC.
  • In vitro co-culture assays using naive CD4+ T cells with sEVs to assess Tfh and Tfr cell differentiation, phenotype, and function.
  • Analysis of cytokine profiles (IL-21, IFN-γ, IL-10).
  • Assessment of the effect of anti-PDL1 antibody treatment.

Main Results:

  • EC patients exhibited lower circulating Tfh, higher circulating Tfr, and reduced Tfh/Tfr ratios compared to HDs.
  • Elevated sEV-PDL1 levels were observed in EC patients and negatively correlated with the Tfh/Tfr ratio.
  • In vitro, sEV-PDL1 inhibited Tfh expansion, promoted Tfr expansion and immunosuppressive functions, and altered cytokine production.
  • Anti-PDL1 antibody treatment reversed the effects of sEV-PDL1.

Conclusions:

  • EC-derived sEV-PDL1 plays a critical role in immunosuppression by disrupting the circulating Tfh/Tfr balance.
  • sEV-PDL1 promotes Tfr cell expansion and function while inhibiting Tfh cells.
  • Targeting sEV-PDL1 represents a promising therapeutic strategy to restore immune balance in esophageal cancer.