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TIGIT Affects CAR NK-cell Effector Function in the Solid Tumor Microenvironment by Modulating Immune Synapse

Ishwar Navin1, Matthew Dysthe2, Prashant S Menon3

  • 1Department of Immunology and Microbiology, Baylor College of Medicine, Houston, Texas.

Cancer Immunology Research
|July 30, 2025
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Summary
This summary is machine-generated.

Deleting the TIGIT receptor from chimeric antigen receptor (CAR)-NK cells enhances their ability to fight solid tumors. This modification improves CAR-NK cell persistence and efficacy in immunosuppressive tumor microenvironments.

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Area of Science:

  • Immunology
  • Cancer Biology
  • Cell Therapy

Background:

  • Chimeric antigen receptor (CAR)-NK cell therapies show promise against blood cancers.
  • Solid tumors create immunosuppressive microenvironments that limit CAR-NK cell effectiveness.
  • The role of TIGIT, an NK cell inhibitory receptor, in CAR-NK cell function against solid tumors is unknown.

Purpose of the Study:

  • To investigate the impact of TIGIT expression on the anti-tumor activity of GD2-targeted CAR-NK cells in solid tumor models.
  • To compare the efficacy of TIGIT-deleted versus TIGIT-expressing CAR-NK cells in immunosuppressive environments.

Main Methods:

  • Co-culture systems and in vivo xenografts mimicking solid tumor microenvironments (TiME) were used.
  • TIGIT-expressing and TIGIT-deleted human GD2.CAR-NK cells were compared for anti-tumor activity, expansion, and persistence.
  • Mechanistic studies explored the role of TIGIT in cell adhesion, synapse formation, and serial killing.

Main Results:

  • TIGIT-deleted GD2.CAR-NK cells demonstrated significant anti-tumor activity, expansion, and persistence in TIGIT ligand-rich tumor environments.
  • TIGIT-expressing CAR-NK cells showed impaired anti-tumor function under similar conditions.
  • TIGIT deletion improved tumor control by downregulating cell adhesion molecules, reducing avidity and synapse duration, enhancing serial killing, and increasing tumor destruction efficiency.

Conclusions:

  • TIGIT plays a novel, non-canonical role in modulating CAR-NK cell activity against solid tumors.
  • Deleting TIGIT from CAR-NK cells can overcome inhibitory receptor-mediated resistance in solid tumors.
  • Targeting TIGIT offers a potential strategy to enhance CAR-NK cell therapy efficacy for solid tumors.