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Induced Expression of B7-1 on Myeloma Cells Following Retroviral Gene Transfer Results in Tumor-Specific Recognition by Cytotoxic T Cells¹

Karin Tarte^*, Xue-Guang Zhang^*,, Eric Legouffe, Catherine Hertog^§, Majid Mehtali^¶, Jean-François Rossi and Bernard Klein^2,*,§

^* Institut National de la Santé et de la Recherche Médicale Unite 475, Montpellier, France; Immunology Research Unit, Suzhou Medical College, Suzhou, China; Service des Maladies du Sang B, Centre Hospitalier Universitaire Montpellier, Hôpital Lapeyronie, Montpellier, France; ^§ Unite de Therapie Cellulaire, Centre Hospitalier Universitaire Montpellier, Hôpital Saint Eloi, Montpellier, France; and ^¶ Transgene, Strasbourg, France

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- plus TNF- 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.

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