Fleer A, Koopman M G, von dem Borne A E, Engelfriet C P
Br J Haematol. 1978 Nov;40(3):439-46. doi: 10.1111/j.1365-2141.1978.tb05815.x.
The mechanism by which human monocytes increase the osmotic fragility of red cells sensitized with Rhesus alloantibodies anti-D was studied in vitro. Both the increase in osmotic fragility and the lysis of red cells by monocytes were enhanced by cytochalasin B and were inhibited by hydrocortisone. These effects were similar to the effects of these agents on lysosomal enzyme release by monocytes. However, hydrocortisone was completely ineffective when added 1 h after mixing monocytes and sensitized red cells. This indicates that the damage responsible for the fragility increase and lysis is completed within 1 h and suggests that it is due to lysosomal enzymes released by the monocytes. Since for the full expression of the osmotic fragility increase and lysis an incubation time much longer than 1 h is required, it appears that the latter phenomena are the non-specific sequelae of damage inflicted upon the red cell by released lysosomal enzymes.
在体外研究了人类单核细胞增加用抗D恒河猴同种抗体致敏的红细胞渗透脆性的机制。细胞松弛素B增强了单核细胞引起的红细胞渗透脆性增加和溶解，而氢化可的松则抑制了这些作用。这些效应与这些药物对单核细胞溶酶体酶释放的作用相似。然而，在单核细胞与致敏红细胞混合1小时后加入氢化可的松则完全无效。这表明导致脆性增加和溶解的损伤在1小时内完成，并提示这是由于单核细胞释放的溶酶体酶所致。由于要充分表达渗透脆性增加和溶解需要比1小时长得多的孵育时间，因此似乎后一种现象是释放的溶酶体酶对红细胞造成损伤的非特异性后遗症。
