Fig. 7.
Fig. 7. A proposed mechanism for IVIG effects on increased antiplatelet antibody clearance. / (1) IVIG (black IgGs) and 7E3 (white IgGs) are taken into the cell by pinocytosis. (2) At physiologic pH, IgG has low affinity for the FcRn receptor, but as the pH decreases following endocytosis, the affinity of IgG for the FcRn receptor increases and the IgG binds to the receptor. Because of the much greater concentrations of IVIG relative to 7E3, IVIG is bound preferentially to the receptor. (3) Bound IgG molecules are protected from release into the lysosome, and (4) eventually returned to the circulation (5). Unbound IgG proceeds to the lysosome (6) where it is catabolized by proteases.

A proposed mechanism for IVIG effects on increased antiplatelet antibody clearance.

(1) IVIG (black IgGs) and 7E3 (white IgGs) are taken into the cell by pinocytosis. (2) At physiologic pH, IgG has low affinity for the FcRn receptor, but as the pH decreases following endocytosis, the affinity of IgG for the FcRn receptor increases and the IgG binds to the receptor. Because of the much greater concentrations of IVIG relative to 7E3, IVIG is bound preferentially to the receptor. (3) Bound IgG molecules are protected from release into the lysosome, and (4) eventually returned to the circulation (5). Unbound IgG proceeds to the lysosome (6) where it is catabolized by proteases.

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