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Exosomes are stable, lipid bilayer-enclosed vesicles capable of crossing biological barriers. They can carry a wide range of molecules required for intercellular communication. Once exosomes are released from the cell where they originated, they enter a recipient cell through various pathways such as fusion, receptor-mediated endocytosis, macropinocytosis, and phagocytosis.
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Intraluminal vesicles (ILVs) are small vesicles 50-80 nm in diameter formed during the maturation of early endosomes. A specialized endosome containing numerous ILVs is called a multivesicular body (MVB). ILVs contain internalized molecules such as antigens, nucleic acids, proteins, and metabolites. Some of these molecules are released from the MVBs inside exosomes and are transported to other cells. Other MVBs contain molecules that are retained in the ILVs and are later degraded within the...
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Related Experiment Video

Updated: Aug 19, 2025

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

Wenqun Zhong, Wei Guo1

  • 1Department of Biology, University of Pennsylvania, Philadelphia, Pennsylvania.

Blood Cancer Discovery
|December 1, 2022
PubMed
Summary

Small extracellular vesicles from chronic lymphocytic leukemia cells suppress anti-tumor immunity. These vesicles alter CD8 T-cell function, hindering the immune response against cancer.

Area of Science:

  • Immunology
  • Oncology
  • Cell Biology

Background:

  • Cancer progression relies on immune evasion.
  • Chronic lymphocytic leukemia (CLL) is a type of blood cancer.
  • Extracellular vesicles play roles in intercellular communication.

Discussion:

  • Small extracellular vesicles (sEVs) from CLL cells were investigated for their impact on antitumor immunity.
  • The study utilized a mouse model of CLL.
  • sEVs were found to inhibit the immune system's ability to fight cancer.

Key Insights:

  • Gargiulo and colleagues demonstrate that sEVs from CLL can impair anti-tumor immune responses.
  • These vesicles affect the transcriptome, proteome, and metabolome of CD8 T-cells.
  • This molecular reprogramming of CD8 T-cells contributes to immune suppression.

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Outlook:

  • Understanding sEVs' role in CLL immune evasion could lead to novel therapeutic strategies.
  • Targeting sEVs may restore CD8 T-cell function and enhance cancer immunotherapy.
  • Further research is needed to explore the therapeutic potential of targeting sEVs in blood cancers.