Some of the molecular events in the complement (C)-mediated solubilization of
immune complexes (IC) have been clarified in recent years. The solubilization is primarily
mediated by alternative C pathway proteins whereas factors in the classical pathway accelerate
the process. Components of the membrane attack complex do not participate in the reaction.
Besides affecting the size and solubility of circulating IC the interaction with C factors
influences the reactivities of the complexes towards fluid phase reactants and mediates the
reversible binding of IC to cellular C3 receptors. Our knowledge of the cellular localization,
expression and structure of the C3 receptors, especially the C3b (CR1) receptor, has been
considerably extended in the last few years, whereas our understanding of the physiological
role of these receptors is still fragmentary. However, it is becoming increasingly evident that
impaired solubilization of IC in patients with compromised C function may permit the complexes
to deviate from their normal pattern of interaction with C3 receptors probably
influencing both the organ distribution and clearance of IC and thereby also their phlogistic
potentials.