Paroli M, Carloni G, Franco A, De Petrillo G, Alfani E, Barnaba V
Fondazione Andrea Cesalpino, I Clinica Medica, Università La Sapienza, Roma, Italy.
Res Virol. 1993 Jul-Aug;144(4):327-32.
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 dependent 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.
在本研究中,我们调查了主要组织相容性复合体(MHC)I类阳性人肝癌细胞系诱导纯化的同种异体CD8+T淋巴细胞原发性增殖反应的能力。我们发现,HA22T/VGH和Li7A细胞系可诱导CD8+T细胞显著增殖,而HepG2细胞则不能,并且这些反应依赖于I类分子的表达。在进行的阻断实验中,为了确定所涉及的共刺激信号,我们发现抗ICAM1单克隆抗体可显著抑制CD8+T细胞的增殖反应。这些发现表明,表达HLA I类分子的转化肝细胞可能通过ICAM1介导的黏附相互作用直接诱导细胞毒性T细胞反应,从而参与抗肿瘤免疫监视。