[Immunological damage to erythrocytes].
The mechanisms by which red cells are destroyed under the influence of antibodies with different immunochemical and biological characteristics are described. It is shown that the interaction of antibody with the red cell per se does not lead to a disturbance of red cell function. Activation of the whole complement system leads to direct lysis of the erythrocyte (complement hemolysis). The fixation of red cells coated with activated C3:C3 receptors on phagocytic cells is another mechanism which leads to red cell destruction. The hypothesis that adherence to the Fc-receptors of phagocytic cells is essential for the destruction of red cells under the influence of noncomplement-binding antibodies is discussed. Arguments in favour of this theory are correlation between the subclass of IgG red cell autoantibodies and the absence or presence of increased hemolysis in the patient and a correlation between the degree to which red cells of patients with this kind of antibody adhere to monocytes in vitro and the degree of hemolysis in the patient. It is shown by in vitro experiments how this adherence process can take place in vivo in the presence of normal plasma IgG although the latter completely inhibits the adherence phenomenon in vitro.
D000906:Antibodies; D001323:Autoantibodies; D001666:Binding Sites, Antibody; D002448:Cell Adhesion; D003080:Cold Temperature; D003176:Complement C3; D003165:Complement System Proteins; D004912:Erythrocytes / Q000276:immunology*; D006461:Hemolysis; D006801:Humans; D007141:Immunoglobulin Fc Fragments; D009000:Monocytes / Q000276:immunology; D010447:Peptide Hydrolases; D010586:Phagocytes / Q000276:immunology
D000906:Antibodies; D001323:Autoantibodies; D003176:Complement C3; D007141:Immunoglobulin Fc Fragments; D003165:Complement System Proteins; D010447:Peptide Hydrolases
Immunologische Schädigung der Erythrozyten