Language

English

Publication Date

11-2-2022

Journal

Cancer Immunology Research

DOI

10.1158/2326-6066.CIR-22-0115

PMID

36122411

PMCID

PMC9633434

PubMedCentral® Posted Date

5-2-2023

PubMedCentral® Full Text Version

Author MSS

Abstract

T-cell immunotherapy has demonstrated remarkable clinical outcomes in certain hematologic malignancies. However, efficacy in solid tumors has been suboptimal, partially due to the hostile tumor microenvironment composed of immune-inhibitory molecules. One such suppressive agent abundantly expressed in solid tumors is Fas ligand (FasL), which can trigger apoptosis of Fas-expressing effector cells such as T cells and natural killer (NK) cells. To alleviate this FasL-induced suppression of tumor-specific immune cells in solid tumors, we describe here the development of a Fas decoy that is secreted by engineered cells upon activation and sequesters the ligand, preventing it from engaging with Fas on the surface of effector cells. We further improved the immune-stimulatory effects of this approach by creating a Fas decoy and IL15 cytokine fusion protein, which enhanced the persistence and antitumor activity of decoy-engineered as well as bystander chimeric-antigen receptor (CAR) T cells in xenograft models of pancreatic cancer. Our data indicate that secreted Fas decoys can augment the efficacy of both adoptively transferred and endogenous tumor-specific effector cells in FasL-expressing solid tumors.

Keywords

Humans, Fas Ligand Protein, T-Lymphocytes, Neoplasms, Tumor Microenvironment, Killer Cells, Natural, Cancer immunotherapy, Adoptive T cell therapy, Chimeric Antigen Receptor, CAR T cells

Published Open-Access

yes

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