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本实验利用小鼠闭合性创伤模型研究了创伤后巨噬细胞对T淋巴细胞增殖的调节作用,并初步探讨了其作用机理。结果显示:创伤后1、2、4、7、10天T淋巴细胞转化活性均明显低于正常,伤后巨噬细胞对T淋巴细胞转化活性的抑制作用增强,以伤后1、2、4 d最为明显。伤后巨噬细胞产生白细胞介素1(IL-1)的能力无明显变化,但产生肿瘤坏死因子(TNF)和前列腺素E_2(PGE_2)的能力却明显增强。体外应用消炎痛(1μg/ml)可以阻断创伤小鼠T淋巴细胞转化活性的受抑状态。丝裂霉素C(25μg/ml)体外处理创伤后巨噬细胞,可以阻断其细胞因子的生成,但不能完全阻断其对T淋巴细胞转化活性的抑制作用。上述结果提示:小鼠闭合性创伤后T淋巴细胞增殖功能的降低,同伤后巨噬细胞的抑制作用有一定关系。创伤后巨噬细胞可通过分泌大量的PGE_2及直接的细胞接触方式发挥其对T淋巴细胞增殖的抑制效应。
In this study, the mouse model of closed trauma was used to study the regulatory effect of traumatic macrophages on the proliferation of T lymphocytes. The mechanism of action was also discussed. The results showed that the transformation activity of T lymphocytes at 1, 2, 4, 7 and 10 days after trauma was significantly lower than that of normal, and the inhibitory effect of macrophages on T lymphocyte transformation activity was enhanced. d the most obvious. The ability of macrophages to produce interleukin-1 (IL-1) did not change significantly after injury, but their ability to produce tumor necrosis factor (TNF) and prostaglandin E2 (PGE2) was significantly enhanced. In vitro application of indomethacin (1 μg / ml) could block the suppressive state of T lymphocyte transformation activity in traumatized mice. Mitomycin C (25μg / ml) treatment of traumatic macrophages in vitro, which can block the formation of cytokines, but can not completely block its inhibitory effect on T lymphocyte transformation. The above results suggest that the decrease of T lymphocyte proliferation after the closed traumatic injury in mice is related to the inhibition of macrophages after injury. Traumatic macrophages can exert their inhibitory effect on the proliferation of T lymphocytes by secreting a large amount of PGE2 and direct cell contact.