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Fig. 3 | Immunity & Ageing

Fig. 3

From: Autoimmune hemolytic anemia: current knowledge and perspectives

Fig. 3

Hemolysis in the course of warm AIHA: the main pathological mechanisms and sites of hemolysis, adapted and modified from Berentsen and Sundic [72]. Antibody-coated RBCs are ingested and degraded by macrophages or destroyed by antibody dependent cell cytotoxicity in the spleen. Some of the erythrocytes are only partially phagocytosed and form microspherocytes which return to the circulation. Microspherocytes have rigid cellular membrane and lack flexibility which causes their sequestration in the spleen. Weak activation of complement by Ig G antibodies leads to extravascular hemolysis in the liver

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