ACCELERATED DECAY OF C3B TO IC3B WHEN C3B IS BOUND TO THE CRYPTOCOCCUS-NEOFORMANS CAPSULE

Incubation of encapsulated and nonencapsulated Cryptococcus neoformans in normal human serum (NHS) leads to activation and binding of potent ially opsonic fragments of complement component C3 to the yeast cells. Analysis of the molecular forms of C3 after incubation of encapsulate d cryptococci in NHS showed that the percentage of bound C3 occurring as iC3b approached 100% after 8 min. The percentage of bound C3 occurr ing as iC3b on nonencapsulated cryptococci never exceeded 70%, even af ter 60 min of incubation in NHS. Conversion of C3b to iC3b was assesse d further by incubating C3b-coated cryptococci for various times with a mixture of complement factors H and I at 40% of their respective phy siological concentrations. Most, if not all, of the C3b on encapsulate d cryptococci was converted to iC3b at a single fast rate. Conversion of C3b to iC3b on nonencapsulated cryptococci did not follow a single rate constant and appeared to have a fast and a slow component. Studie s of the requirements for factors H and I in cleavage of C3b to iC3b s howed steep dose-response curves for both factors in the case of encap sulated cryptococci and shallow curves with C3b bound to nonencapsulat ed cryptococci. Taken together, our results indicate that C3b molecule s bound to encapsulated cryptococci have a uniformly high susceptibili ty to conversion to iC3b by factors H and I. In contrast, a significan t portion of the C3b bound to nonencapsulated cryptococci is very resi stant to conversion to iC3b by factors H and I.