Nanoplastics can be ingested by organisms and penetrate biological barriers to affect multiple physiological functions. However, few studies have focused on the effects of nanoplastics on the mammalian immune system. We evaluated the effects and underlying mechanism of nanoplastics of varying particle sizes and surface charges on murine splenic lymphocytes. We found that nanoplastics penetrated into splenic lymphocytes and that nanoplastics of a diameter of 50 nm were absorbed more efficiently by the cells. The nanoplastics decreased cell viability, induce cell apoptosis, up-regulated apoptosis-related protein expression, elicited the production of reactive oxygen species, altered mitochondrial membrane potential, and impaired mitochondrial function. Positively charged nanoplastics exerted the strongest toxicity. Negatively charged and uncharged nanoplastics caused oxidative stress and mitochondrial structural damage in lymphocytes, while positively charged nanoplastics induced endogenous apoptosis directly. Moreover, nanoplastics inhibited the expression of activated T cell markers on the T cell surface, while inhibiting the differentiation of CD8⁺ T cells and the expression of helper T cell cytokines. In terms of the mechanism, a series of key signaling molecules in the pathways of T cell activation and function were markedly down-regulated after exposure to nanoplastics.

纳米塑料可以被生物体摄取并穿透生物屏障以影响多种生理功能。然而，很少有研究关注纳米塑料对哺乳动物免疫系统的影响。我们评估了不同粒径和表面电荷的纳米塑料对小鼠脾淋巴细胞的影响和潜在机制。我们发现纳米塑料渗透到脾淋巴细胞中，并且直径为 50 nm 的纳米塑料更有效地被细胞吸收。纳米塑料降低细胞活力，诱导细胞凋亡，上调凋亡相关蛋白表达，引发活性氧物质的产生，改变线粒体膜电位和线粒体功能受损。带正电的纳米塑料具有最强的毒性。带负电荷和不带电荷的纳米塑料引起淋巴细胞的氧化应激和线粒体结构损伤，而带正电荷的纳米塑料直接诱导内源性细胞凋亡。此外，纳米塑料抑制了 T 细胞表面活化 T 细胞标志物的表达，同时抑制了 CD8 的分化。⁺ T 细胞和辅助 T 细胞细胞因子的表达。在机制方面，T细胞活化和功能通路中的一系列关键信号分子在暴露于纳米塑料后显着下调。