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Evidences for a "New" C1 Inhibitor, Factor S, Released from Leucocytes

Sloan-Kettering Institute, New York, N. Y. and National Institutes of Health, Bethesda, Md.

Abstract

Pretreatment of sheep erythrocytes (E) with supernatants of short-term cultures of mouse spleen or thymus cells induces the following interactions with guinea pig complement: 1) Supernatant pretreated EAlim (S.EAlim) are less susceptible to lysis by excess complement. S.EAC4 yield a lower C2 titer, have an increased Tmax, but an unchanged C2 decay when compared with medium-pretreated EAC4. Lysis of already formed EACis not inhibited. Therefore the inhibition affects C2 activation. 2) E, pretreated with supernatant (S.E), are able to fix C, as detected by transfer to EAC4: In order to generate the same number of C-fixing sites by using IgM hemolysins, five to six times the optimal amount is required. Yet S.EC cannot be lysed by the other components added in excess. S.EC can remove C4 from the fluid phase with the same efficiency as EIgMC but S.EC treated with C4 cannot remove C2. 3) Native C binds to S.E: S.E and EIgM remove C1 from the fluid phase with the same efficiency; fixation of on S.E is decreased after incubation with native C