Fusions of Human Ovarian Carcinoma Cells with Autologous or Allogeneic Dendritic Cells Induce Antitumor Immunity

Human ovarian carcinomas express the CA-125, HER2/neu, and MUC1 tumor-associated Ags as potential targets for the induction of active specific immunotherapy. In the present studies, human ovarian cancer cells were fused to human dendritic cells (DC) as an alternative strategy to induce immunity agai...

Full description

Saved in:
Bibliographic Details
Published inThe Journal of immunology (1950) Vol. 165; no. 3; pp. 1705 - 1711
Main Authors Gong, Jianlin, Nikrui, Najmosama, Chen, Dongshu, Koido, Shigeo, Wu, Zekui, Tanaka, Yasuhiro, Cannistra, Stephen, Avigan, David, Kufe, Donald
Format Journal Article
LanguageEnglish
Published United States Am Assoc Immnol 01.08.2000
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Human ovarian carcinomas express the CA-125, HER2/neu, and MUC1 tumor-associated Ags as potential targets for the induction of active specific immunotherapy. In the present studies, human ovarian cancer cells were fused to human dendritic cells (DC) as an alternative strategy to induce immunity against known and unidentified tumor Ags. Fusions of ovarian cancer cells to autologous DC resulted in the formation of heterokaryons that express the CA-125 Ag and DC-derived costimulatory and adhesion molecules. Similar findings were obtained with ovarian cancer cells fused to allogeneic DC. The fusion cells were functional in stimulating the proliferation of autologous T cells. The results also demonstrate that fusions of ovarian cancer cells to autologous or allogeneic DC induce cytolytic T cell activity and lysis of autologous tumor cells by a MHC class I-restricted mechanism. These findings demonstrate that fusions of ovarian carcinoma cells and DC activate T cell responses against autologous tumor and that the fusions are functional when generated with either autologous or allogeneic DC.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.165.3.1705