Enhancement of B cell function as antigen-presenting cell during interplay with Th cells.

We have previously reported that C57BL/6 mouse B cells present Ag to an I-Ab-restricted and OVA-specific T cell clone, 34-7F, to secrete IL-2 but not to proliferate, whereas spleen adherent cells as APC induce a proliferative response of 34-7F cells to OVA. In this T cell response, it was examined whether B cells were stimulated during presenting Ag and acquired the ability as APC to induce proliferative Ag-response of 34-7F cells. For this aim, B cells prepared from unstimulated mouse spleen cells were cultured with 34-7F cells in the presence of OVA and then compared with unstimulated B cells for APC function in the OVA-response of 34-7F cells. Unstimulated B cells proliferated when cultured for 2 days with irradiated 34-7F cells and OVA, and the proliferation was inhibited by an anti-I-Ab mAb. B cells which had been stimulated for 2 days with 34-7F cells and OVA induced an increase in phosphatidyl inositol metabolism in 34-7F cells in the presence of Ag, whereas unstimulated B cells failed to do so. The increase was dependent on the dose of OVA and on the number of the stimulated B cells. Ag presentation by the stimulated B cells (but not by unstimulated ones), also induced IL-2R expression on 34-7F cells, which resulted in IL-2-dependent proliferation. The IL-2R expression does not depend on the possible increase in IL-2 production by the T cells, inasmuch as the activated B cells induced lower expression of IL-2 mRNA or lower secretion of IL-2 by 34-7F cells than that induced by unstimulated B cells. These results suggest that B cells receive signal(s) from 34-7F cells to enhance APC function during Ag-presentation to the T cells which do not proliferate in the response to Ag on unstimulated B cells, and that the stimulated B cells induce the proliferative response of 34-7F cells to OVA.