闭合性创伤小鼠巨噬细胞对T淋巴细胞增殖的影响

Effects of macrophages on T lymphocyte proliferation after closed trauma in mice

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。

A murine closed trauma model was used to study the modulating effects of macrophages on T lymphocyte proliferation and the mechanism.It was found that the T lymphocyte transformation was significantly lower than the control on the 1st,2nd,4th,7th and 10 day posttrauma and the suppression of macrophages on T lymphocytes was augmented especially on the 1st,2nd and 4th day posttrauma.Interleukin 1 production of macrophages was not obviously changed while tumor necrosis factor and prostaglandin E2 synthesis were significantly increased.Indomethacin 1μg/ml could block the suppression of macrophages on T cell transformation and mitomycin-C 25μg/ml could stop the synthesis of cytokine but could not block completely the suppression on T cell transformation.These findings suggest that closed trauma induced suppression on T cell transformation results from macrophages through the release of large amounts of prostaglandin E2 and direct cell to cell contact.