Allogeneic interactions in the immune response and tolerance. II. Mechanism of stimulation of TNP plaque forming cells in normal rats

The mechanism of increase in trinitrophenyl-specific plaque forming cells in F₁ rats injected with parental lymphoid cells was studied. T cells seem to be necessary in the donor allogeneic lymphoid cell inoculum. In contrast, thymus-deprived F₁ recipients (B rats) were found to respond as well to allogeneic stimulation as thymus repopulated rats (B + T). Since the host provides the precursors of trinitrophenyl plaqueforming cells in this graft-versus-host situation, this suggests that allogeneic T cells induce B cells of the recipient to proliferate. This possibility was investigated by injecting normal rats with E. coli lipopolysaccharide, a potent B cell mitogen. A shortlived increase in trinitrophenyl-specific plaque-forming cells was elicited by 10 μg native E. coli lipopolysaccharide or by 2 mg detoxified E. coli lipopolysaccharide. Treatment of donor cells with mitomycin C or actinomycin D prevented the stimulation of trinitrophenyl plaque-forming cells in F₁ hosts. Thus, both DNA and RNA synthesis are necessary for this allogeneic effect.