In the present study, we investigated the ability of major histocompatibility complex (MHC) class-I+ human hepatoma cell lines to induce primary proliferative responses of purified allogeneic CD8+ T lymphocytes. We found that HA22T/VGH and Li7A, but not HepG2 cells induced significant proliferation of CD8+ T cells and that these responses were depedent on class I molecule expression. In blocking experiments carried out to identify the costimulatory signals involved, we found that anti-ICAM1 monoclonal antibodies drastically inhibited CD8+ T-cell proliferative responses. These findings suggest that transformed hepatocytes expressing HLA class I molecules may participate in anti-tumour immunosurveillance by the direct induction of cytotoxic T-cell responses through ICAM1-mediated adhesive interaction.
HUMAN HEPATOMA-CELLS EXPRESSING HLA CLASS-I MOLECULES STIMULATE PRIMARY RESPONSES OF PURIFIED CD8+ T-LYMPHOCYTES / Paroli, Marino; G., Carloni; A., Franco; G., De Petrillo; E., Alfani; Barnaba, Vincenzo. - In: RESEARCH IN VIROLOGY. - ISSN 0923-2516. - 144:4(1993), pp. 327-332.
HUMAN HEPATOMA-CELLS EXPRESSING HLA CLASS-I MOLECULES STIMULATE PRIMARY RESPONSES OF PURIFIED CD8+ T-LYMPHOCYTES
PAROLI, Marino;BARNABA, Vincenzo
1993
Abstract
In the present study, we investigated the ability of major histocompatibility complex (MHC) class-I+ human hepatoma cell lines to induce primary proliferative responses of purified allogeneic CD8+ T lymphocytes. We found that HA22T/VGH and Li7A, but not HepG2 cells induced significant proliferation of CD8+ T cells and that these responses were depedent on class I molecule expression. In blocking experiments carried out to identify the costimulatory signals involved, we found that anti-ICAM1 monoclonal antibodies drastically inhibited CD8+ T-cell proliferative responses. These findings suggest that transformed hepatocytes expressing HLA class I molecules may participate in anti-tumour immunosurveillance by the direct induction of cytotoxic T-cell responses through ICAM1-mediated adhesive interaction.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.