Zier K S, Gansbacher B
Division of Clinical Immunology, Mount Sinai School of Medicine, New York, NY 10029, USA.
J Mol Med (Berl). 1996 Mar;74(3):127-34. doi: 10.1007/BF01575444.
The identification of tumor-associated antigens has focused attention on the mechanisms that underlie the failure of T cells to destroy tumor cells. A deeper understanding of the process of signal transduction following the binding of ligand by the T cell receptor can help to identify underlying defects that may be involved. Gene therapy using tumor cells genetically modified to express cytokines or surface determinants is a promising technique for stimulating antitumor responses. A potential pitfall in its application to cancer, however, is that some patients' T cells are immune suppressed and may resist stimulation by such genetically engineered vaccines. Recent studies have demonstrated that T cells from tumor-bearing patients exhibit abnormalities in signal transduction events, possibly rendering them unable to respond to activation signals. Gene therapy with interleukin 2 secreting tumor cells in an animal model has been shown effective in preventing the onset of signaling defects. A more precise definition of the molecular mechanisms that enable cytokine-secreting tumor cells to stimulate specific antitumor responses may make it feasible to optimize immunotherapeutic approaches resulting in better clinical results.
肿瘤相关抗原的鉴定使人们将注意力集中在T细胞无法摧毁肿瘤细胞的潜在机制上。深入了解T细胞受体与配体结合后的信号转导过程,有助于识别可能涉及的潜在缺陷。利用基因改造后的肿瘤细胞来表达细胞因子或表面决定簇进行基因治疗,是一种很有前景的刺激抗肿瘤反应的技术。然而,将其应用于癌症治疗时,一个潜在的问题是,一些患者的T细胞受到免疫抑制,可能会抵抗这种基因工程疫苗的刺激。最近的研究表明,荷瘤患者的T细胞在信号转导事件中表现出异常,这可能使它们无法对激活信号作出反应。在动物模型中,用分泌白细胞介素2的肿瘤细胞进行基因治疗已被证明可有效预防信号缺陷的发生。更精确地定义使分泌细胞因子的肿瘤细胞能够刺激特异性抗肿瘤反应的分子机制,可能会使优化免疫治疗方法变得可行,从而带来更好的临床效果。