Role of B cells in the stimulation of syngeneic mixed lymphocyte responses.

Two different approaches were used to examine the role of B cells in the stimulation of syngeneic MLR. The relative inability of spleen and peritoneal exudate cells from B cell deficient mice, treated with anti-mu from birth, to serve as stimulator cells in SMLR was previously shown in SJL mice and confirmed in BALB/c mice in the present studies. Preincubation of cells from anti-mu treated mice with serum Ig does not enhance their ability to stimulate. Upon stimulation with normal spleen cells responses from anti-mu treated mouse T cells are not deficient. Responses of thymus cells from neonates and from adult cortisone-treated mice are also much higher when the splenic stimulator cells come from normal rather than from anti-mu treated mice. The deficiency of the stimulator cells from anti-mu treated mice is in the high density cell population as obtained after BSA gradient fractionation of collagenase treated lymph node or spleen fragments. Low density populations from anti-mu treated and normal mice stimulate equally well. Addition of exogenous IL-2 to the cultures enhances the syngeneic MLR to all stimulator populations and allows stimulation by spleen cells from anti-mu treated mice. It is concluded that, while B cells represent the major stimulator cell population in whole spleen cell suspensions, other accessory cells (dendritic cells?) are more efficient, possibly synergize with B cells by producing IL-1, but usually represent only a minor subpopulation. The other approach concerns the effectiveness of SMLR stimulation by several tissue culture, cloned B lymphoma cell lines, and by a transplantable BALB/c B lymphoma. Of the five stimulating lymphoma cell lines only one stimulates approximately as well in the absence as in the presence of polyethylene glycol. These latter cells (A20.1.11) can also stimulate T cell proliferation and IL-2 production in the absence of Ia+ accessory cells in the responding population and, therefore, either produce their own IL-1 or are able to bypass the requirement for this lymphokine.