Phagocytosis is a well-known characteristic of activated macrophages and the ability of activated microglia to phagocytose debris during neuroinflammation has been shown, for example, by the demonstration within microglia of amyloid fibrils in AD (McGeer et al., 1992; Wisniewski, Vorbrodt, Wegiel, Morys, & Lossinsky, 1990), myelin fragments in multiple sclerosis (Krogsgaard et al., 2000), and in animal models such as produced by injection of glutamate into the arcuate nucleus (Pelaez, Blazquez, Pastor, Sanchez, & Amat, 1999). An essential element in the phagocytic process is identification of targets by labeling with either the complement fragments C3b and C4b and thus engaging microglial complement receptors or by specific antibodies that facilitate phagocytosis via microglial Fc receptors. C3b may also interact with IgG present in the area of complement activation. The C3b-IgG dimers are more potent opsonins than C3b alone.
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