IMMUNOREGULATION IN VIVO AND IN VITRO BY CYTOKINES

以前，我们已经证明了干扰素-α与IL-2在 淋巴因子激活的杀伤细胞(LAK)在不同疾病中的扩增 老鼠的隔间。LAK细胞的增殖和扩增 观察每个细胞对干扰素-α和 IL-2治疗。这些观察结果表明，银杏叶提取物的抗肿瘤作用 干扰素-α和IL-2可能是通过激活LAK细胞介导的。这个 联合应用干扰素-γ和IL-2可增加LAK活性 未被证明具有协同抗肿瘤作用。其他效应器 如CTL、巨噬细胞和未知细胞群可能与 观察到的两种干扰素的差异。此外，我们还有 观察到IL-6可引起小鼠淋巴样细胞增殖 小鼠的脾。这些细胞似乎是T淋巴细胞，因为没有 照射组和裸鼠均可见细胞增殖。 增殖细胞不具有NK或LAK活性，但继发性 IL-6可诱导CTL活性。

Previously, we have demonstrated that IFN-alpha synergizes with IL-2 in the augmentation of lymphokine activated killer (LAK) cells in various compartments of mice. Both proliferation and augmentation of LAK cell activity on a per cell basis was observed in response to IFN-alpha and IL-2 therapy. These observations suggest that anti-tumor effects of IFN-alpha with IL-2 may be mediated through activation of LAK cells. The administration of IFN-gamma with IL-2 increased LAK activity while it has not been shown to cause synergistic anti-tumor effects. Other effectors such as CTL, macrophages and unknown cell population may be responsible for differences observed with the two interferons. Additionally, we have observed that IL-6 causes the proliferation of lymphoid cells in the spleen of mice. These cells appear to be T lymphocytes because no proliferation was observed in the irradiated and nude mice. Proliferating cells did not bear NK or LAK activity, however, secondary CTL activity was induced by IL-6.