Related Experiment Video
Updated: Jun 10, 2026

A Syngeneic Mouse B-Cell Lymphoma Model for Pre-Clinical Evaluation of CD19 CAR T Cells
Published on: October 16, 2018
NKG2D-based CAR-T cells for synovial sarcoma: A preclinical proof-of-concept study
Tomohiro Miyazaki1, Yudai Murayama2, Naoki Oike2
1Department of Pediatrics, Graduate School of Medical and Dental Sciences, Niigata University, Niigata 951-8510, Japan; Division of Orthopedic Surgery, Graduate School of Medical and Dental Sciences, Niigata University, Niigata 951-8510, Japan.
Abstract:
The prognosis for advanced synovial sarcoma remains poor, with limited therapeutic options. Recently, cloned T cell receptor (TCR)-engineered T cell therapy has shown promising results in patients with advanced synovial sarcoma; however, the number of patients eligible for this therapy is limited owing to human leukocyte antigen (HLA) restriction. To solve this problem, we focused on chimeric antigen receptor (CAR)-T cells that target ligands of NKG2D, an activating receptor of natural killer cells. Because NKG2D recognizes a family of eight ligands, we hypothesized that NKG2D-based CARs could function as an intrinsic multi-antigen targeting platform, potentially mitigating antigen heterogeneity and antigen escape, which are key barriers in CAR-T therapy for solid tumors. We first evaluated the surface expression of NKG2D ligands (NKG2DLs) in synovial sarcoma cell lines and examined their transcript levels in public bulk RNA-seq datasets from synovial sarcoma tissues. We then constructed NKG2D-based, 4-1BB-co-stimulated CAR-T cells. These CAR-T cells showed effector responses and antitumor effects against synovial sarcoma cells in vitro, as demonstrated by the results of the intracellular cytokine production, cytokine secretion, CD107a degranulation assay, WST-8 assay, and real-time cell analysis, and in vivo in an NSG mouse xenograft model of synovial sarcoma. Although further mechanistic, translational, and safety validation studies are required, these findings provide a preliminary disease-specific preclinical proof of concept for HLA-independent NKG2D-based CAR-T cell therapy in synovial sarcoma, particularly in patients who are ineligible for or have not responded to TCR-T therapy.
Insights
Chimeric antigen receptor (CAR)-T cell therapy targeting NKG2D ligands shows promise for synovial sarcoma. This HLA-independent approach offers a potential new treatment for patients ineligible for or unresponsive to T cell receptor (TCR)-T therapy.
Area of Science:
- Oncology
- Immunotherapy
- Cell Therapy
Background:
- Advanced synovial sarcoma has a poor prognosis and limited treatment options.
- Current T cell receptor (TCR)-engineered T cell therapy is HLA-restricted, limiting patient eligibility.
- Chimeric antigen receptor (CAR)-T cell therapy offers a potential alternative.
Purpose of the Study:
- To investigate the potential of NKG2D-ligand targeting CAR-T cells as an HLA-independent therapy for synovial sarcoma.
- To evaluate NKG2D-ligand expression in synovial sarcoma.
- To assess the in vitro and in vivo efficacy of NKG2D-based CAR-T cells against synovial sarcoma.
Main Methods:
- Assessed NKG2D ligand (NKG2DL) surface expression and transcript levels in synovial sarcoma.
- Constructed NKG2D-based, 4-1BB-co-stimulated CAR-T cells.
- Evaluated CAR-T cell effector functions and anti-tumor effects in vitro and in vivo using a mouse xenograft model.
Main Results:
- NKG2DLs were expressed in synovial sarcoma cell lines and tissues.
- NKG2D-based CAR-T cells demonstrated effector responses and anti-tumor activity against synovial sarcoma in vitro.
- NKG2D-based CAR-T cells exhibited anti-tumor effects in vivo in a synovial sarcoma xenograft model.
Conclusions:
- NKG2D-based CAR-T cell therapy is a potential HLA-independent treatment for synovial sarcoma.
- This approach may overcome antigen heterogeneity and escape, key challenges in solid tumor CAR-T therapy.
- Further validation is needed, but this study provides a preclinical proof of concept for a novel synovial sarcoma therapy.

