Figure 5.
Summary of the mechanism of immunomodulation by the (G2)2 glycoform of IgG. In autoimmune/inflammatory state, hypogalactosylated, fucosylated serum IgG cannot compete with high-avidity multimeric IgG immune complexes on a target cell for FcγRIIIa binding, resulting in the activation of an effector cell (left). Increased levels of galactosylated, nonfucosylated serum IgG by administration of the (G2)2 glycoform of IVIG result in saturation of FcγRIIIa with the (G2)2 glycoform, inhibiting the activation of an effector cell (right). E, effector cell. Tg, target cell. Gal, galactose. Fuc, fucose.