Splenic uptake of immune complexes in man is complement-dependent.

摘要: We have examined the effects of hereditary homozygous C2 deficiency on processing radiolabeled soluble immune complexes (IC). A patient with was studied before and after treatment fresh frozen plasma (FFP). Hepatitis B surface Ag (HBsAg):anti-HBsAg were prepared in vitro using 123I, injected intravenously. Dynamic static gamma-scintigraphy performed to delineate sites kinetics complex clearance. The initially when her level CH50 zero, again 1 wk later 12 units FFP, which normalized these parameters. Before there rapid uptake by liver (t90% [time for 90% uptake] = 13.6 min) clearance from circulation (t1/2 6.8 min). No splenic detected, no binding erythrocyte CR1. Between 30 60 min release 11% tracer liver. In second study, normalization classical pathway complement activity, t1/2 IC increased 9.8 min, t90% 27 min. Twenty percent now localized spleen, longer any between this posttherapy study closely similar two normal subjects parallel, a maximum 72% erythrocytes. These observations indicate that spleen humans is complement-dependent, suggest observed predisposition SLE patients may be related abnormal complexes.