Enhanced cytotoxicity of IFN-gamma-producing CD4+ cytotoxic T lymphocytes specific for T. gondii-infected human melanoma cells.
Enhanced cytotoxicity of IFN-gamma-producing CD4+ cytotoxic T lymphocytes specific for T. gondii-infected human melanoma cells.
复制标题
增强产生 IFN-γ 的 CD4 细胞毒性 T 淋巴细胞的细胞毒性，该淋巴细胞对刚地弓形虫感染的人黑色素瘤细胞具有特异性。
作者：
Tian;F. Aosai;K. Norose;M. Ueda;A. Yano
从慢性弓形虫病患者的PBL中建立了对弓形虫感染的人黑素瘤P36细胞特异的CD 4+细胞系。用T细胞每周体外刺激获得CD4 + CTL细胞株。感染了弓形虫的P36细胞与患者共享HLA-DR4分子。结果表明，CD4 + CTL细胞株对T.感染弓形虫的P36或T.抗HLA-DR单克隆抗体对刚地氏感染的自身EB病毒转化B淋巴瘤（EBV-Ya）有明显的抑制作用，而抗HLA-A、B、C单克隆抗体则不能阻断其裂解活性。因此，CD4 + CTL细胞系对T.感染弓形虫的P36受HLA-DR分子的限制。在响应Ag特异性刺激，CD4 + CTL系产生显著水平的IFN-γ。外源性IFN-γ可上调T细胞表面MHCII类分子的表达，但不能上调I类分子的表达。感染P36细胞。此外，T.当靶细胞与IFN-γ共培养时，刚地氏感染的P36细胞增加。这些数据表明，CD4 + CTL介导的抗T.刚第虫感染的黑素细胞通过IFN-γ的自分泌产生而增强。此外，CD4 + CTL可能通过杀伤T.刚第虫感染的黑色素细胞
CD4+ lines specific for Toxoplasma gondii-infected human melanoma P36 cells were established from PBL of a patient with chronic toxoplasmosis. CD4+ CTL lines were obtained by weekly in vitro stimulation with T. gondii-infected P36 cells that shared HLA-DR4 molecules with the patient. The lytic activity of CD4+ CTL lines against T. gondii-infected P36 or T. gondii-infected autologous EBV-transformed B lymphoma (EBV-Ya) was inhibited by anti-HLA-DR mAb, whereas anti-HLA-A, B, C mAb failed to block the lytic activity. Thus, the cytotoxicity of CD4+ CTL lines against T. gondii-infected P36 was restricted by HLA-DR molecules. In response to Ag-specific stimulation, CD4+ CTL lines produced significant levels of IFN-gamma. Exogenously added IFN-gamma up-regulated the surface expression of MHC class II, but not of class I in T. gondii-infected P36 cells. In addition, the CTL activity against T. gondii-infected P36 cells was augmented when target cells were co-cultured with IFN-gamma. These data indicate that CD4+ CTL-mediated cytotoxicity against T. gondii-infected melanocytes is enhanced by the autocrine production of IFN-gamma. Further, CD4+ CTL may play a role in the manifestation of toxoplasmic retinochoroiditis by killing T. gondii-infected melanocytes.