The inhibition of the cytotoxicity of NK cells by microgravity in space is of serious concern to the health of astronauts. However, there remains a lack of in-depth research into the mechanisms of action of this suppression. In the present study, the effects of simulated microgravity (SMG) on the morphology, survival rate and the ability of NK cells to kill were studied initially and then the mechanism of SMG in the inhibition of NK cytotoxicity was preliminarily investigated from the perspectives of stimulatory and inhibitory receptor expression. Further, the present study attempted to reveal the molecular mechanisms of SMG inhibition of the stimulatory receptor NKG2D from the perspective of DNA methylation and the expression of its adaptor protein DAP10. The results demonstrated that down-regulation of stimulatory receptor NKG2D expression and significantly up-regulated expression of inhibitory receptor CD158a may be important in explaining for the inhibition of NK cell cytotoxicity by SMG. The down-regulation of DAP10 expression, and not its DNA methylation, that is the possible cause of the down-regulation of NKG2D expression by SMG and the subsequent suppression of NK cell activity. However, inhibition of DAP10 expression by SMG was also not achieved by influencing methylation, and so additional analysis of the mechanism is required. The results of the present study lay the foundations for finally elucidating the molecular mechanisms by which microgravity leads to a decline in NK cell activity and contributes important evidence for interpreting the regulatory mechanisms of NK cell cytotoxicity.

太空中的微重力抑制NK细胞的细胞毒性与宇航员的健康密切相关。但是，仍然缺乏对这种抑制作用机理的深入研究。在本研究中，首先研究了模拟微重力（SMG）对形态，存活率和NK细胞杀伤能力的影响，然后从刺激性的角度初步研究了SMG抑制NK细胞毒性的机制。和抑制性受体表达。此外，本研究试图从DNA甲基化及其衔接蛋白DAP10的表达来揭示SMG抑制刺激受体NKG2D的分子机制。结果表明，刺激性受体NKG2D表达的下调和抑制性受体CD158a的显着上调对于解释SMG抑制NK细胞的细胞毒性可能是重要的。DAP10表达的下调，而不是其DNA甲基化，这可能是SMG下调NKG2D表达并随后抑制NK细胞活性的可能原因。但是，通过影响甲基化也无法实现SMG对DAP10表达的抑制作用，因此需要对该机理进行进一步分析。本研究的结果为最终阐明微重力导致NK细胞活性下降的分子机制奠定了基础，并为解释NK细胞细胞毒性的调控机制提供了重要证据。