The Fc-receptor function of human mononuclear phagocyte system: physiological role, alteration in immune diseases and modulation

Circulating immune complexes (CIC) are detectable in high titer in patients with various immune
diseases and the deposition of these complexes is believed to be important in the pathogenesis of
these disorders. The reticuloendothelial system (RES), which includes the KuptTer cells of the liver and the splenic macrophages, is involved in the removal of CIC from the vascular system. A defect in CIC clearance may enhance their tissue deposition. Accordingly, during the past few years, increased interest has been devoted to the measurement of immune clearance mediated by receptors for Fc, IgG coated autologous red blood cells (IgG-RBC) labelled with 51Cr have been used as immune tracer particles to follow the Fc-receptor function of whole RES in normal and pathological conditions. Prolonged clearance times of IgG-RBC are generally found in most immune complex-mediated diseases. Using IgG-RBC labelled with 99m Tc, it has been thereafter possible to determine not only the clearance half-time of the tracer, but also separated spleen and liver Fc-receptor binding capacities. It has been clearly demonstrated that the spleen to liver
ratios per surface area (S/L s) are deeply pathological in immune disorders, even when clearance
half-times (T 1/2) remain within the normal range. Abnormal ratios result from both a decreased splenic uptake and an increased liver uptake of IgG-RBC, this "hepatic compensation" preventing the T 1/2 to be out of the normal values. Abnormal T 1/2 are therefore observed only when the spleen and liver phagocytic capacities are saturated. The splenic Fc-receptor blockade is generally correlated with the disease activity and, less frequently, with the immune complex plasma levels. Serial measurements of S/Ls may be therefore of clinical interest by delineating those patients in whom the evolutivity of the disease is potentially high. Finally, serial S/Ls measurements have allowed the in vivo study of the modulation of the macrophagic Fc-receptor function by plasma exchange, corticosteroid administration and highdose gammaglobulin infusion.