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[Hemolytic anemia, myocardial infarction and xenotransplantation: what do they have in common?]
1Medizinische Universitätsklinik B, Kantonsspital Basel.
Complement is activated by antibodies, by necrotic cells and by the many surfaces which do not inhibit the amplification loop of the alternative pathway. Examples of such activation include hyperacute rejection in xenotransplantation models (antibody), myocardial infarction (necrotic cells) and paroxysmal nocturnal hemoglobinuria (PNH: lack of complement control on abnormal erythrocytes and platelets). Over the past decade many of the complement regulatory proteins have been described, analyzed and produced in recombinant forms. One of these proteins is complement receptor 1 (CR1, CD35), which in soluble form is capable of inhibiting complement activation in vivo. In many experimental models, soluble CR1 has been shown to reduce antibody-mediated damage, diminish inflammation at the time of cell necrosis and inhibit lysis of PNH cells. For the first time it will be possible to inhibit complement activation in humans.
Complement is activated by antibodies, by necrotic cells and by the many surfaces which do not inhibit the amplification loop of the alternative pathway. Examples of such activation include hyperacute rejection in xenotransplantation models (antibody), myocardial infarction (necrotic cells) and paroxysmal nocturnal hemoglobinuria (PNH: lack of complement control on abnormal erythrocytes and platelets). Over the past decade many of the complement regulatory proteins have been described, analyzed and produced in recombinant forms. One of these proteins is complement receptor 1 (CR1, CD35), which in soluble form is capable of inhibiting complement activation in vivo. In many experimental models, soluble CR1 has been shown to reduce antibody-mediated damage, diminish inflammation at the time of cell necrosis and inhibit lysis of PNH cells. For the first time it will be possible to inhibit complement activation in humans.