Induced Expression of B7-1 on Myeloma Cells Following Retroviral Gene Transfer Results in Tumor-Specific Recognition by Cytotoxic T Cells
| Autor: | Karin Tarte, Zhang, Xg, Legouffe, E., Hertog, C., Mehtali, M., Rossi, Jf, Klein, B. |
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| Rok vydání: | 1999 |
| Předmět: |
Cytotoxicity
Immunologic Immunology Gene Transfer Techniques Antigen-Presenting Cells Epitopes T-Lymphocyte Lymphocyte Activation Retroviridae Antigens Neoplasm HLA Antigens B7-1 Antigen Tumor Cells Cultured Humans Immunology and Allergy Lymphocyte Culture Test Mixed Multiple Myeloma Cell Adhesion Molecules Aged T-Lymphocytes Cytotoxic |
| Zdroj: | Web of Science |
| ISSN: | 1550-6606 0022-1767 |
| DOI: | 10.4049/jimmunol.163.1.514 |
| Popis: | The aim of this study was to evaluate whether tumor cells from patients with multiple myeloma activate allogeneic and autologous T cells. Results showed that myeloma cells expressed few B7-2 and no B7-1 in six cell lines and primary cells from 11 patients. They expressed substantial levels of HLA class I, CD40, and a set of adhesion molecules. In accordance with the low density of B7 molecules on these cells, they were poor allogeneic CD8+ T cell stimulators. Neither IFN-γ plus TNF-α nor CD40 stimulation significantly induced B7-1 or up-regulated B7-2 on human myeloma cell line or primary myeloma cells from six of seven patients. However, such induction was found on autologous bone-marrow nontumoral cells and on autologous dendritic cells following CD40 stimulation. High B7-1 expression was stably obtained on human myeloma cell line using transduction with a B7-1 retrovirus, enabling these cells to stimulate allogeneic CD8+, though not CD4+, T cell proliferation. For one patient with advanced disease, B7-1 gene transfer made it possible to amplify autologous cytotoxic T cells that killed autologous myeloma cells in an HLA class I-restricted manner, but not autologous PHA blasts. These results suggest that B7-1 gene transfer could be a promising immunotherapeutic approach in multiple myeloma. |
| Databáze: | OpenAIRE |
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