Zier K S, Gansbacher B
Division of Clinical Immunology, Mount Sinai School of Medicine, New York, NY 10029, USA.
Hum Gene Ther. 1995 Oct;6(10):1259-64. doi: 10.1089/hum.1995.6.10-1259.
Studies of signal transduction by T cells are slowly identifying the intracellular messengers that must be generated for full T cell activation to take place. The recent, convincing identification of several tumor-associated antigens (TAA) has transformed our task into trying to define the mechanisms that underlie the failure of T cells to destroy antigenic tumor cells. Although there are a variety of hypotheses that explain why tumors grow progressively, even if they are antigenic, recent evidence suggests that T cells from tumor-bearing patients exhibit abnormalities in signal transduction that render them unable to respond to appropriate activation signals, even following proper stimulation. Gene therapy with interleukin-2 (IL-2)-secreting tumor cells in an animal model has been effective in preventing the onset of these signaling defects. Discovery of the molecular mechanisms by which such cytokine-secreting tumor cells induce immune responses and how they may best be applied clinically may provide clearer indications of the directions to pursue to alter the balance between the T cell and the tumor cell in the patient's favor.
对T细胞信号转导的研究正在逐步确定充分激活T细胞所必需的细胞内信使。最近,几种肿瘤相关抗原(TAA)的确凿鉴定,将我们的任务转变为试图确定T细胞无法破坏抗原性肿瘤细胞背后的机制。尽管有多种假说解释肿瘤为何会逐渐生长,即使它们具有抗原性,但最近的证据表明,荷瘤患者的T细胞在信号转导方面存在异常,即使在受到适当刺激后,它们也无法对适当的激活信号作出反应。在动物模型中,用分泌白细胞介素-2(IL-2)的肿瘤细胞进行基因治疗,已有效地预防了这些信号缺陷的发生。发现此类分泌细胞因子的肿瘤细胞诱导免疫反应的分子机制,以及如何将它们最佳地应用于临床,可能会更清楚地指明为使患者体内T细胞与肿瘤细胞之间的平衡向有利于患者的方向改变而应追寻的方向。