IMMUNOREGULATION IN VIVO AND IN VITRO BY CYTOKINES

细胞因子的体内和体外免疫调节

• 批准号: 3792449
• 负责人: R PURI
• 金额: --
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/3792449
• 关键词: cytokine; cytotoxic T lymphocyte; immunoregulation; interferons; interleukin 2; interleukin 6; laboratory mouse; leukocyte activation /transformation; lymphocyte proliferation; lymphokine activated killer cell; tissue /cell culture

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.

以前，我们已经证明IFN-α与IL-2协同作用， 淋巴因子激活的杀伤（LAK）细胞的增加， 老鼠的房间 LAK细胞的增殖和增强 在每个细胞的基础上观察到对IFN-α的应答活性， IL-2治疗。 这些观察结果表明， IFN-α与IL-2可能通过激活LAK细胞介导。 的 IFN-γ与IL-2联合给药可增加LAK活性， 没有显示出引起协同抗肿瘤作用。 其他效应物 例如CTL、巨噬细胞和未知细胞群可能是导致 观察到的两种干扰素的差异。 此外，我们还有 观察到IL-6引起淋巴细胞在淋巴细胞中的增殖， 小鼠脾脏。 这些细胞似乎是T淋巴细胞，因为没有 在照射和裸鼠中观察到增殖。 淋巴细胞不具有NK或LAK活性，但是， IL-6诱导CTL活性。