Department of Nephrology and Blood Purification, Kidney Disease Center, Tokyo Medical University Hachioji Medical Center, Tokyo 193-0998, Japan.
Division of Critical Care and Emergency Medicine, Tokyo Medical University Hachioji Medical Center, Tokyo 193-0998, Japan.
Int J Mol Sci. 2023 Aug 5;24(15):12465. doi: 10.3390/ijms241512465.
Although experimental models have shown that the innate immune system is a main contributor to acute kidney injury (AKI), its involvement in human sepsis-associated AKI (SA-AKI) remains unclear. We retrospectively evaluated 19 patients with SA-AKI who were treated with continuous renal replacement therapy (CRRT). Serum cytokine, complement components, and the proportion and functions of innate immune cells, such as CD56 T cells, CD56 natural killer (NK) cells, and monocytes, were analyzed. There were no differences in the proportions of CD56 T and NK cells between patients with SA-AKI and healthy controls. In patients with SA-AKI, fas ligand (FasL) expression in CD56 T cells was significantly upregulated, and the proportion of perforin-positive CD56 T cells tended to be higher than that in healthy controls. The positive rate of both FasL and perforin of CD56 T cells was significantly higher than that of CD56 T cells, which include cytotoxic T cells. Antigen-presenting capacity and phagocytic activity of monocytes in patients with SA-AKI were significantly decreased compared to those of healthy controls and did not recover soon after the initiation of CRRT. CD56 T cells are involved in the disease processes of human SA-AKI through effector molecules such as FasL or perforin.
虽然实验模型表明，固有免疫系统是急性肾损伤（AKI）的主要贡献者，但它在人类脓毒症相关 AKI（SA-AKI）中的参与仍不清楚。我们回顾性评估了 19 例接受连续肾脏替代治疗（CRRT）的 SA-AKI 患者。分析了血清细胞因子、补体成分以及固有免疫细胞（如 CD56 T 细胞、CD56 自然杀伤（NK）细胞和单核细胞）的比例和功能。SA-AKI 患者和健康对照组之间 CD56 T 和 NK 细胞的比例没有差异。在 SA-AKI 患者中，CD56 T 细胞中 Fas 配体（FasL）的表达明显上调，且穿孔素阳性 CD56 T 细胞的比例趋于高于健康对照组。CD56 T 细胞中 FasL 和穿孔素的阳性率均明显高于包括细胞毒性 T 细胞在内的 CD56 T 细胞。与健康对照组相比，SA-AKI 患者的单核细胞的抗原呈递能力和吞噬活性显著降低，并且在开始 CRRT 后不久并未很快恢复。CD56 T 细胞通过 FasL 或穿孔素等效应分子参与人类 SA-AKI 的疾病过程。
