IN SITU ANTITUMOR IMMUNITY AND EFFECTS OF RADIATION

本研究的目的是评价其作用机制 阻止免疫系统控制恶性细胞 增长 三个潜在的重要机制将是 考察 第一，I类组织相容性抗原的作用 肿瘤细胞在产生免疫中的表达将是 使用自发性小鼠肺肿瘤（第1行）进行评估，该肿瘤 无法表达这些正常抗原 放射治疗 似乎诱导这些抗原的表达， 对这种肿瘤的免疫反应的重要意义， 放疗后。 第二，据了解， 肿瘤内的低氧细胞是有效治疗的限制性特征， 放射治疗 这种缺氧的存在是因为 肿瘤生长超过血液供应，类似于在体内发现的肿瘤。 多细胞肿瘤球体，一个模型系统， 体内实体瘤的特征。 我们将利用这一模式， 确定缺氧是否也影响细胞溶解功能， T淋巴细胞。 第三，我们已经确定了一种免疫抑制剂， 由自发性鼠乳腺肿瘤产生的因子（IIF）， 抑制B和T细胞增殖的EMT 6。 我们 将进一步表征功能和生化 该因子的性质，并确定其在体内的意义。

The ojbective of this research is to evaluate the mechanisms which prevent the immune system from controlling malignant cell growth. Three potentially important mechanisms will be examined. First, the role of class I histocompatibility antigen expression by tumor cells in generating immunity will be evaluated using a spontaneous murine lung tumor, line 1, which fails to express these normal antigens. Radiation treatment appears to induce expression of these antigens, which may have important implications for the immune response to this tumor, subsquent to radiotherapy. Second, it is known that the presence of hypoxic cells within tumors is a limiting feature in effective radiation treatment. This hypoxia, which exists because many tumors outgrow the blood supply, is similar to that found within multicellular tumor spheroids, a model system which has many characteristics of in vivo solid tumors. We will use this model to determine whether hypoxia also affects the function of cytolytic T lymphocytes. Third, we have identified an immunoinhibitory factor (IIF) produced by a spontaneous murine mammary tumor, EMT6 which inhibits the proliferation of both B and T cells. We will further characterize the functional and biochemical properties of this factor and determine its in vivo significance.