Microenvironment actuated CAR T cells improve solid tumor efficacy without toxicity

Sci Adv. 2025 Jan 24;11(4):eads3403. doi: 10.1126/sciadv.ads3403. Epub 2025 Jan 22.

Abstract

A major limiting factor in the success of chimeric antigen receptor (CAR) T cell therapy for the treatment of solid tumors is targeting tumor antigens also found on normal tissues. CAR T cells against GD2 induced rapid, fatal neurotoxicity because of CAR recognition of GD2+ normal mouse brain tissue. To improve the selectivity of the CAR T cell, we engineered a synthetic Notch receptor that selectively expresses the CAR upon binding to P-selectin, a cell adhesion protein overexpressed in tumor neovasculature. These tumor microenvironment actuated T (MEAT) cells ameliorated T cell infiltration in the brain, preventing fatal neurotoxicity while maintaining antitumor efficacy. We found that conditional CAR expression improved the persistence of tumor-infiltrating lymphocytes because of enhanced metabolic fitness of MEAT cells and the infusion of a less differentiated product. This approach increases the repertoire of targetable solid tumor antigens by restricting CAR expression and subsequent killing to cancer cells only and provides a proof-of-concept model for other targets.

MeSH terms

  • Animals
  • Antigens, Neoplasm / immunology
  • Cell Line, Tumor
  • Humans
  • Immunotherapy, Adoptive* / methods
  • Lymphocytes, Tumor-Infiltrating / immunology
  • Lymphocytes, Tumor-Infiltrating / metabolism
  • Mice
  • Neoplasms / immunology
  • Neoplasms / pathology
  • Neoplasms / therapy
  • Receptors, Antigen, T-Cell / genetics
  • Receptors, Antigen, T-Cell / immunology
  • Receptors, Antigen, T-Cell / metabolism
  • Receptors, Chimeric Antigen* / genetics
  • Receptors, Chimeric Antigen* / immunology
  • Receptors, Chimeric Antigen* / metabolism
  • T-Lymphocytes* / immunology
  • T-Lymphocytes* / metabolism
  • Tumor Microenvironment* / immunology
  • Xenograft Model Antitumor Assays

Substances

  • Receptors, Chimeric Antigen
  • Antigens, Neoplasm
  • Receptors, Antigen, T-Cell