Figure 3
Figure 3. Hypothetical model for cytoadhesion of parasitized RBCs to blood group A or group B structures. Infected RBCs expressing PfEMP-1 can bind to group A (or to a lesser extent, group B) determinants on other cells. In the left panel, cytoadhesion from lectin-binding fails to occur because of the absence of group A or group B antigens. In the center panel, an infected RBC adheres to an uninfected RBC (homotypic adherence) via A or B antigens. The infected cell in turn adheres to endothelium either by binding to blood group antigen on endothelial cells or by binding to blood group antigens on platelets or VWF (heterotypic adherence). In the right panel, cytoadherence is blocked by soluble blood group substance present in the plasma of group A and/or B individuals with the Le(a−b−) Secretor phenotype. Copyright Kimberly Main Knoper; used with permission.

Hypothetical model for cytoadhesion of parasitized RBCs to blood group A or group B structures. Infected RBCs expressing PfEMP-1 can bind to group A (or to a lesser extent, group B) determinants on other cells. In the left panel, cytoadhesion from lectin-binding fails to occur because of the absence of group A or group B antigens. In the center panel, an infected RBC adheres to an uninfected RBC (homotypic adherence) via A or B antigens. The infected cell in turn adheres to endothelium either by binding to blood group antigen on endothelial cells or by binding to blood group antigens on platelets or VWF (heterotypic adherence). In the right panel, cytoadherence is blocked by soluble blood group substance present in the plasma of group A and/or B individuals with the Le(a−b−) Secretor phenotype. Copyright Kimberly Main Knoper; used with permission.

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