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目的探讨Tim-3信号影响免疫细胞抗感染作用的机制。方法通过基因芯片筛选及体内外验证的方法探讨Tim-3对IFI44(一种抗感染关键效应分子)表达的影响,并结合H1N1感染模型对其意义进行评价。结果在巨噬细胞上敲低Tim-3表达或通过Tim-3融合蛋白阻断Tim-3信号,均能显著提高IFI44的表达,而在Tim-3高表达的巨噬细胞中IFI44的表达受到明显抑制。在整体水平上检测Tim-3信号对IFI44表达的影响发现,给予受H1N1病毒感染小鼠腹腔注射s Tim-3蛋白能显著提高小鼠体内IFI44的表达进而降低H1N1病毒载量。结论 Tim-3在抑制抗病毒感染效应分子IFI44表达中发挥关键作用;部分解释了Tim-3调控抗感染免疫的机制,也为防治H1N1等病毒的感染提供了新的思路。
Objective To investigate the mechanism of Tim-3 signal affecting the anti-infective effect of immune cells. Methods The effect of Tim-3 on the expression of IFI44, an anti-infection key effector molecule, was explored by gene chip screening and in vitro and in vivo validation, and its significance was evaluated in combination with H1N1 infection model. Results The knockdown of Tim-3 expression on macrophages or the blockade of Tim-3 signaling by Tim-3 fusion protein significantly increased the expression of IFI44, whereas the expression of IFI44 was up-regulated in Tim-3-overexpressing macrophages Obvious inhibition. To detect the effect of Tim-3 signal on the expression of IFI44, we found that intraperitoneal injection of Tim-3 protein in mice infected with H1N1 virus can significantly increase the expression of IFI44 in mice and then reduce the H1N1 viral load. Conclusion Tim-3 plays a key role in inhibiting the expression of IFI44, an anti-viral infection effector molecule. It partially explains the mechanism by which Tim-3 regulates anti-infective immunity and provides a new idea for preventing and treating H1N1 infection.