FC-RECEPTORS IN LIVER SINUSOIDAL ENDOTHELIAL-CELLS IN NZB W F1 LUPUS MICE - A HISTOLOGICAL ANALYSIS USING SOLUBLE IMMUNOGLOBULIN G-IMMUNE COMPLEXES AND A MONOCLONAL-ANTIBODY (2.4G2)/

In systemic lupus erythematosus accompanied by the abnormal appearance of circulating immune complexes (ICs), Fc gamma receptor (FcR)-mediat ed IC handling in macrophages including Kupffer cells has been shown p reviously. However, sinusoidal endothelial cells (SECs) largely ingest soluble immunoglobulin (Ig) G-ICs through FcRs. In this study, the ch aracter, antigenic expression, and activity (i.e., ligand-binding capa city of SEC FcRs in NZB/NZW F1 lupus and NZW nonautoimmune mice) were immunohistochemically analyzed using monoclonal antibody (MAb) 2.4G2 t o FcRs and peroxidase-antiperoxidase IgG as a ligand on cryosections. MAb 2.4G2 stained SECs and blocked the ligand binding of SEC FcRs in b oth mice strains. The staining intensities with MAb 2.4G2 in SECs and the FcR activities in SECs alone and all sinusoidal cells in both mice strains reached their maximum values at the age of 5 months. Staining intensities in NZB/W F1 were significantly higher at 1 and 2 months a nd lower at 9 months than those in NZW. The number of Kupffer cells de tected by MAb F4/80 to macrophages in both mice strains gradually incr eased until 5 months, but their number in NZB/W F1 at 9 months was twi ce as large as that in NZW. In conclusion, SEC FcRs in mice are low-af finity FcRs that react with MAb 2.4G2. The data of FcR activity sugges t no impairment of the FcR-mediated IgG-IC binding on SECs in NZB/W F1 in early life. However, at the late stage of the disease, despite an increased number of Kupffer cells, the capacity of FcR-mediated IgG-IC handling in liver may be reduced by the decreased FcR activity in all sinusoidal cells including SECs and Kupffer cells.