Immune complexes can activate either the classical or the alternative complement pathway. The classical pathway plays a major role in maintaining immune complexes in a soluble form, preventing their deposition in tissues. C3b bound to the solubilized immune complexes promotes their clearance by the erythrocyte complement receptor CR1. If the rate of immune complex formation exceeds the ability to clear these complexes via Fc receptors and CR1, the immune complexes can deposit within tissues, leading to inflammation. This efficient immune complex transport and removal by Fc and complement receptors can be overwhelmed, however, leading to tissue deposition and immune complex disease. This situation may result from overproduction of immune complexes, blockade of phagocytosis by the reticuloendothelial system, or complement depletion resulting in inefficient solubilization of immune complexes.