The capacity of serum to support deposition of C3, properdin and factor B was studied by enzyme‐linked immunosorbent assay using solid‐phase immune complexes (IC) for activation of complement. Deposition of C3 and properdin occurred in fairly dilute normal human serum (NHS), but factor B uptake was hardly detectable. Alternative pathway‐mediated deposition of C3 with slow kinetics was demonstrated in C2‐deficient serum and in NHS depleted of C1q, factor D and properdin (C1qDP‐depleted serum) after reconstitution with factor D and properdin. Efficient uptake of properdin required a functional classical pathway, in the presence of which C3 and properdin were rapidly deposited onto the IC. Judging from findings in C3‐deficient serum, factor I‐deficient serum, and C1qDPB‐depleted serum, the uptake of properdin was strictly C3‐dependent, and did not require the presence of factors B and D. Thus, C3b fixed to IC was the principal ligand for properdin in the assay. The findings could have biological implications relating to complement‐mediated modification of immune complexes in disease.