Twenty-five long-term B-cell lines were studied for B-BCGF activity. The cell lines were cultured in the presence or absence of the new
tumor promoter teleocidin, and control and
teleocidin-treated derived supernatants were cocultured with purified B cells obtained from healthy donors and patients with B
chronic lymphatic leukemia (B-CLL), in the presence of anti-mu. In attempt to delineate the role of other B-cell
lymphokines in promoting proliferation of activated B cells, the supernatants were also studied for
interleukin 1 (IL-1),
interleukin 2 (IL-2), and
interferon gamma (IFN-gamma). The effect of B-cell-derived
lymphokines on the proliferation of activated B cells obtained from the 14 donors was heterogeneous, and three types of response were observed: In four healthy donors there was induction of B-cell proliferation by B-cell
lymphokines derived from both control cells and
teleocidin-treated cells. In cells obtained from the other five healthy donors there was induction of B-cell proliferation by B-cell
lymphokines derived from
teleocidin-treated cells. In the five B-CLL patients, B-cell proliferative response to B-cell
lymphokines derived from both control cells and
teleocidin-activated cells was absent. Comparison of B-BCGF reactivity to T-BCGF reactivity demonstrated that B-CLL B lymphocytes did not respond to either B-BCGF or T-BCGF, whereas normal B cells responded to T-BCGF and may proliferate upon stimulation with B-cell-derived
IL-2 and/or B-BCGF. These results suggest heterogeneity of B-BCGF receptor reactivity in B lymphocytes derived from healthy donors, and lack of both B-BCGF and T-BCGF receptor reactivities in B lymphocytes derived from B-CLL patients; B-cell-derived
lymphokines influence normal B-cell response but not leukemic B cells; B-BCGF optimal effect is in large part due to other B-cell
lymphokines, especially B-cell-derived IL-2; the possible existence of various B-BCGFs.