Böhle A, Thanhäuser A, Ulmer A J, Mattern T, Ernst M, Flad H D, Jocham D
Department of Urology, Medical University of Lübeck, Germany.
Urol Res. 1994;22(3):185-90. doi: 10.1007/BF00571848.
Previously we had shown that, upon activation with viable bacillus Calmette-Guérin (BCG), peripheral blood mononuclear cells (PBMNC) could be rendered cytotoxic against otherwise insensitive natural killer (NK)-resistant bladder cancer cell lines. This phenomenon had been termed the BCG-activated killer (BAK) cell phenomenon. By means of depletion and enrichment procedures of mononuclear cell subpopulations derived from BCG-activated PBMNC we further characterized the cytolytic BAK effector cells functionally in an in vitro cytotoxicity assay against the bladder carcinoma cell line BT-A and phenotypically in their pathway of activation. Neither macrophages nor CD4+ T-helper/inducer cells exerted cytotoxic BAK activity. This cytotoxicity was restricted to the CD8+CD56+ subpopulation of T-cytotoxic/NK cells. Furthermore, activation of BAK cells via interferon gamma (IFN-gamma) was evidenced by the complete inhibition of BAK cell generation with an IFN-gamma antibody.
此前我们已经表明，在用活卡介苗（BCG）激活后，外周血单个核细胞（PBMNC）可对原本不敏感的自然杀伤（NK）抗性膀胱癌细胞系产生细胞毒性。这种现象被称为卡介苗激活杀伤（BAK）细胞现象。通过对卡介苗激活的PBMNC衍生的单个核细胞亚群进行去除和富集程序，我们在针对膀胱癌细胞系BT-A的体外细胞毒性试验中进一步从功能上对溶细胞性BAK效应细胞进行了表征，并在其激活途径上从表型上进行了表征。巨噬细胞和CD4 + T辅助/诱导细胞均未发挥细胞毒性BAK活性。这种细胞毒性仅限于细胞毒性/T杀伤性NK细胞的CD8 + CD56 +亚群。此外，通过用γ干扰素（IFN-γ）抗体完全抑制BAK细胞生成，证明了通过IFN-γ激活BAK细胞。
