Abstract
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 in vivo, they are either haemolysed immediately, or, due to an unknown factor, escape direct haemolysis. In the latter case β1E and β1A disappear from the cell membrane. To the sites where these proteins have been attached once, no new β1E or β1A molecules can be bound. Full complement activation thus becomes impossible.
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