Asaka M, Iida H, Izumino K, Sasayama S
Second Department of Internal Medicine, Faculty of Medicine, Toyama Medical and Pharmaceutical University, Japan.
Nephron. 1988;49(4):291-5. doi: 10.1159/000185078.
We investigated the natural killer (NK) cell activity of peripheral blood mononuclear cells (PBMC) and the suppressive factor of NK cell activity in patients on maintenance hemodialysis (HD). NK cell activity was significantly lower in patients on HD than in healthy controls (20.2 +/- 16.5 vs. 31.0 +/- 13.2%, p less than 0.01). There was no difference in NK cell activity between patients treated with cuprophane and high-permeability membrane. NK cells from patients on HD showed a poor response to interleukin-2, and uremic sera significantly suppressed NK cell activity of normal PBMC. Although urea, creatinine, methylguanidine or guanidinosuccinic acid alone did not suppress the NK cell activity of normal PBMC, the guanidino compound did so significantly. It is suggested that defective NK cell activity in uremic patients explains in part their susceptibility to malignancy and infection. The immunosuppressive effect may be exhibited by synergism or mosaic of uremic toxins.
我们研究了维持性血液透析（HD）患者外周血单个核细胞（PBMC）的自然杀伤（NK）细胞活性以及NK细胞活性的抑制因子。HD患者的NK细胞活性显著低于健康对照（20.2±16.5对31.0±13.2%，p<0.01）。用铜仿膜和高通透性膜治疗的患者之间NK细胞活性无差异。HD患者的NK细胞对白介素-2反应较差，尿毒症血清显著抑制正常PBMC的NK细胞活性。虽然单独的尿素、肌酐、甲基胍或胍基琥珀酸不抑制正常PBMC的NK细胞活性，但胍基化合物可显著抑制。提示尿毒症患者NK细胞活性缺陷部分解释了他们对恶性肿瘤和感染的易感性。免疫抑制作用可能由尿毒症毒素的协同作用或镶嵌作用表现出来。
