Mononuclear phagocytes in the lymph nodes, spleen, and liver then ingest and degrade the complexes. This mode of transport presumably protects vascular endothelium from immune complex-mediated damage. Several factors facilitate the transfer of immune complexes from red blood cells to RES phagocytes in the spleen and liver. Phagocytes possess more CR1 receptors than do red blood cells. Large opsonized complexes are efficiently cleared from the blood in minutes.
Small complexes are poor complement activators and can continue to circulate for many days.
Several processes stimulate the local release of vasoactive substances that increase vascular permeability. C5a generated during complement activation, or the immune complexes by themselves cause platelets to clump, degranulate, and release histamine and serotonin. All of these factors facilitate deposition of immune complexes in blood vessel walls and migration of complexes into tissues. Deposition can occur anywhere in the body, but lesions tend to localize in areas where platelets adhere most often to vascular endothelium because of high blood pressure and turbulence. Several additional factors may explain why some organs, such as the kidney, are affected more frequently than other organs.