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In Vivo Immunogenicity Screening of Tumor-Derived Extracellular Vesicles by Flow Cytometry of Splenic T Cells
08:02

In Vivo Immunogenicity Screening of Tumor-Derived Extracellular Vesicles by Flow Cytometry of Splenic T Cells

Published on: September 23, 2021

Danger fuels immune escape

Massimo Russo1, Santiago Zelenay2

  • 1Cancer Inflammation and Immunity, Cancer Research UK Manchester Institute, University of Manchester, Manchester, UK.

Immunity
|July 14, 2026
PubMed

Insights

Extracellular ATP (eATP) acts as a danger signal in tumors. It activates cancer cell receptor P2RY2, leading to immune suppression and resistance to immunotherapy via the COX-PGE2 pathway.

Area of Science:

  • Immunology
  • Cancer Biology
  • Molecular Signaling

Background:

  • Extracellular ATP (eATP) is recognized as a danger signal that modulates immune responses.
  • The tumor microenvironment harbors complex signaling networks that influence cancer progression and immune evasion.

Purpose of the Study:

  • To elucidate the role of extracellular ATP (eATP) in mediating immune suppression within the tumor microenvironment.
  • To identify the specific receptor and downstream pathway through which eATP exerts its effects on cancer cells and immune cells.

Main Methods:

  • Analysis of signaling pathways in cancer cells.
  • Investigation of receptor-ligand interactions.
  • Assessment of immune cell function in the presence of eATP and its downstream mediators.

Main Results:

  • Extracellular ATP (eATP) signals through the P2RY2 receptor on cancer cells.
  • Activation of P2RY2 triggers the cyclooxygenase-prostaglandin E2 (COX-PGE2) pathway.
  • This pathway results in immune suppression and resistance to immunotherapy.

Conclusions:

  • eATP is identified as a key upstream signal driving prostaglandin E2 (PGE2) expression in the tumor microenvironment.
  • Targeting the eATP-P2RY2-COX-PGE2 axis presents a potential therapeutic strategy to overcome immune suppression and enhance immunotherapy efficacy.

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