Engelfriet C P, Von dem Borne A E, Beckers D, Reynierse E, Van Loghem J J
Clin Exp Immunol. 1972 Jun;11(2):255-64.
Experiments are described the results of which sustain the hypothesis that resistance against complement haemolysis, which is a characteristic of the red cells of patients with chronic cold agglutinin disease, is due to the following mechanism: when red cells react with cold auto-agglutinins , they are either haemolysed immediately, or, due to an unknown factor, escape direct haemolysis. In the latter case βE and βA disappear from the cell membrane. To the sites where these proteins have been attached once, no new βE or βA molecules can be bound. Full complement activation thus becomes impossible.
慢性冷凝集素病患者红细胞所具有的抗补体溶血特性,是由以下机制所致:当红细胞与冷凝集素发生反应时,它们要么立即被溶血,要么由于一个未知因素而逃避直接溶血。在后一种情况下,βE和βA从细胞膜上消失。在这些蛋白质曾经附着过的位点,无法再结合新的βE或βA分子。因此完全补体激活变得不可能。