Previous findings were extended by characterizing the serum clearance and tissue uptake of model soluble immune complexes and the saturation of the RES by these complexes in normal mice and in mice with murine lupus (NZB/W F1 females). Adult NZB/W or young C3H mice were injected with radiolabeled stable site-specifically cross-linked mouse anti-DNP oligomers as model immune complexes to probe RES function. Blood clearance and uptake by liver, spleen and kidney were unimpaired in NZB/W mice. To determine if the RES exhibits partial saturation in the NZB/W mice, a state of RES blockade was induced with heat-aggregated human .gamma.-globulin (HAG). With increasing doses of HAG (1-4 mg/20 g body wt) both strains similarly showed a progressive increase in RES saturation as measured by reduced liver uptake of model oligomers. Recovery from saturation was complete by 120 min in both strains. At maximal liver saturation there was only a small increase in oligomer uptake by kidney or spleen, the majority of complexes remaining within the circulation. RES capacity for handling soluble model immune complexes appears unimpaired in NZB/W mice.
