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Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
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Cytotoxic T cells are a vital component of the immune system. They have the remarkable ability to identify and target antigens on infected or abnormal cells. These antigens often originate from intracellular pathogens such as viruses or abnormal proteins cancer cells produce.
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Engineering CAR-Vδ2 T cells to boost persistence and anti-tumor function.

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Summary
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Engineered CAR-Vδ2 T cells with membrane-bound IL-18 signaling support show enhanced anti-tumor activity. A novel Fas88 fusion protects cells from death, improving persistence for cancer immunotherapy.

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Area of Science:

  • Immunology
  • Cell Therapy
  • Cancer Research

Background:

  • Chimeric antigen receptor (CAR)-modified Vδ2 T cells show promise for cancer immunotherapy.
  • Clinical efficacy is limited by short *in vivo* persistence and susceptibility to activation-induced cell death (AICD).
  • Insufficient cytokine support contributes to limited T cell persistence.

Purpose of the Study:

  • To enhance the *in vivo* persistence and anti-tumor activity of CAR-Vδ2 T cells.
  • To identify membrane-bound cytokines supporting superior CAR-Vδ2 T cell function.
  • To develop a strategy for antigen-driven IL-18 signaling and AICD resistance.

Main Methods:

  • Comparison of membrane-bound (mb) cytokines to identify optimal support for CAR-Vδ2 T cells.
  • Fusion of MyD88 (IL-18R signaling mediator) to an extracellular Fas domain (Fas88) for antigen-driven signaling.
  • Evaluation of Fas88-armed CAR-Vδ2 T cells in xenograft models of hematologic and solid malignancies.

Main Results:

  • Membrane-bound IL-18 (mbIL-18) demonstrated superior anti-tumor activity for CAR-Vδ2 T cells *in vitro* and *in vivo*.
  • Fas88 fusion enabled antigen stimulation-induced IL-18 signaling and protected Vδ2 T cells from AICD.
  • Fas88-armed CAR-Vδ2 T cells exhibited superior, stimulation-dependent *in vivo* expansion and functional persistence.

Conclusions:

  • IL-18 signaling and AICD resistance are critical for CAR-Vδ2 T cell efficacy.
  • A single-transgene modification using Fas88 enhances CAR-Vδ2 T cell activity.
  • This strategy limits inflammatory risk and facilitates clinical translation of CAR-Vδ2 T cell therapy.