Trastuzumab enhanced the cytotoxicity of Vγ9Vδ2 T cells against zoledronate-sensitized osteosarcoma cells

Int Immunopharmacol. 2015 Sep;28(1):160-7. doi: 10.1016/j.intimp.2015.06.002. Epub 2015 Jun 10.

Abstract

Preliminary studies of Vγ9Vδ2 T cells and zoledronate (ZOL) present promising reasons to exploit their immunotherapeutic potential for osteosarcoma treatment (OS). ZOL is a third-generation aminobisphosphonate (ABP) and is well established in the management of cancer-induced bone disease. However, ZOL is characterized by high tropism for bone matrix, and the efficacy of ZOL for sensitizing tumors remains to be optimized. Vγ9Vδ2 T cells are important effectors of antibody-dependent cell-mediated cytotoxicity (ADCC). In this study, we investigated whether Vγ9Vδ2 T cell-mediated killing of ZOL-pretreated OS cells could be increased by the anti-HER-2 monoclonal antibody trastuzumab (TTZ). The cytotoxic activity of Vγ9Vδ2 T cells against osteosarcoma was assessed by an MTS assay in the presence or absence of TTZ. A CD107a assay was used to measure degranulation in cytotoxic Vγ9Vδ2 T cells. Blocking studies were used to determine the effect of relative ligands on Vγ9Vδ2 T cell recognition. TTZ induced an ADCC response in the OS cell line, U2OS; however, it had no effect on another OS cell line HOS with low levels of surface HER2 expression. Although the OS cells pretreated with ZOL for clinically relevant time periods (2hours) stimulated a suboptimal immune response of Vγ9Vδ2 T cells, TTZ could further enhance the cytotoxicity of Vγ9Vδ2 T cells. These results demonstrate that combining TTZ and ZOL significantly increases the cytotoxic potential of Vγ9Vδ2 T cells. This study raises the possibility of utilizing ZOL and TTZ in Vγ9Vδ2 T cell-based immunotherapy for OS.

Keywords: ADCC; Monoclonal antibodies; Osteosarcoma; Trastuzumab; Vγ9Vδ2 T cells; Zoledronate.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Bone Density Conservation Agents / pharmacology*
  • Bone Neoplasms / pathology*
  • Cell Degranulation / drug effects
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cytotoxicity, Immunologic / drug effects*
  • Diphosphonates / pharmacology*
  • Humans
  • Imidazoles / pharmacology*
  • Osteosarcoma / pathology*
  • Receptor, ErbB-2 / genetics
  • T-Lymphocytes, Cytotoxic / drug effects*
  • Trastuzumab / pharmacology*
  • Zoledronic Acid

Substances

  • Antineoplastic Agents
  • Bone Density Conservation Agents
  • Diphosphonates
  • Imidazoles
  • Zoledronic Acid
  • ERBB2 protein, human
  • Receptor, ErbB-2
  • Trastuzumab