Further studies on the ability of regressor sera to block cell-mediated destruction of Rous sarcomas.

Abstract

AbstractPrevious studies have shown that most sera from Japanese quails with growing sarcomas induced by the Schmidt‐Ruppin strain of the Rous virus (SR‐RSV) can block cell‐mediated destruction of Rous sarcoma cells in vitro, and that sera from some quails whose Rous sarcomas have spontaneously regressed (regressors) also have that ability. Six regressor sera, previously shown to be blocking when added to the mixture of target and effector (=regressor spleen) cells in vitro, were tested for blocking effect at either the target or the effector cell level. Three sera could block only when incubated with the target cells, while three other sera blocked at both the target cell and the effector cell level. Two of three regressor sera which had previously been shown to be unblocking (abrogating the blocking activity of progressor sera when mixed with these in vitro) increased cell‐mediated cytotoxicity at a low dilution (potentiation) but had a slight blocking activity at dilution 1:128–1:512, which disappeared upon further dilution. The blocking effect seen at these dilutions appeared to occur at the target cell level and was not detectable after incubation of the effector cells with serum. After incubation of the target cells for 24 h with one of these two regressor sera diluted 1:256, a blocking activity detectable at the effector cell level appeared in the culture medium. The blocking activity of serum from bursectomized progressors (previously reported) increased, after regressor serum diluted 1:16 had been added to it; at that dilution, the regressor serum had no blocking activity by itself. More concentrated regressor serum, on the other hand, was unblocking, i.e. it decreased the blocking activity of serum from bursectomized progressors. The data are compatible with the hypothesis that the blocking factors operating in this system are complexes between antigens released from the tumor and antibodies formed by the host (and, occasionally, free antigen).