Fontana A, Hengartner H, de Tribolet N, Weber E
J Immunol. 1984 Apr;132(4):1837-44.
Studies were designed to investigate whether the cellular immunodeficiency state observed in human glioblastoma patients could be due to inhibitory factors released by the tumor cells. Cultured human glioblastoma cells were found to secrete an interleukin 1-like factor (m.w. 22,000) and a factor (m.w. 97,000) that inhibits interleukin 2 (IL 2)-dependent T cell mechanisms. This is demonstrated by its inhibitory effect on the IL 2-induced proliferation of T cell clones and on the induction of alloreactive cytotoxic T cells in mixed lymphocyte cultures. Additionally the glioblastoma cell-derived 97,000-m.w. factor inhibited growth of neuroblasts but not of fibroblasts and thus shares the characteristics of the neuroblast growth inhibition factor (NGIF) previously detected in the supernatant of fetal rat glia cell cultures. If released by glioblastoma cells in vivo, the factor may contribute to impaired immunosurveillance and to the cellular immunodeficiency state detected in the patients.
开展了多项研究,以调查在人类胶质母细胞瘤患者中观察到的细胞免疫缺陷状态是否可能归因于肿瘤细胞释放的抑制因子。研究发现,培养的人类胶质母细胞瘤细胞可分泌一种白细胞介素1样因子(分子量22,000)和一种抑制白细胞介素2(IL-2)依赖性T细胞机制的因子(分子量97,000)。这可通过其对IL-2诱导的T细胞克隆增殖以及对混合淋巴细胞培养中同种异体反应性细胞毒性T细胞诱导的抑制作用得到证明。此外,胶质母细胞瘤细胞衍生的分子量97,000的因子可抑制神经母细胞的生长,但不抑制成纤维细胞的生长,因此具有先前在胎鼠神经胶质细胞培养上清液中检测到的神经母细胞生长抑制因子(NGIF)的特征。如果该因子在体内由胶质母细胞瘤细胞释放,则可能导致免疫监视受损以及患者中检测到的细胞免疫缺陷状态。