Normal human peripheral blood lymphocytes were shown to activate complement in normal human serum (NHS). This activation led to C3 fixation on the cell membrane, which in turn was visualized by fluorescence. The reaction occurred in the absence of detectable amounts of antibodies, since an agammaglobulinemic patient's serum also supported complement activation, and the results were unaltered by absorption of normal human serum. Trypsin treatment of lymphocytes to remove possible complement activators bound to the cell membrane, did not have any effect on the complement activation by lymphocytes. Complement membrane fluorescence was abolished in the presence of EDTA or ethyleneglycolbis(aminoethylether) tetraacetate (EGTA) supplemented by Mg++ions indicating that the classical pathway of complement activation was involved in the reaction. Experiments performed with T and B-purified populations showed that the phenomenon was confined to the B cell fraction. Complement deposition did not diminish the number of EAC rosettes, and viability remained unchanged after exposure of lymphocytes to normal human serum.