CROSS-TALK BETWEEN T-CELL AND B-CELL GENERATES B-ANTIGEN-PRESENTING CELLS ABLE TO INDUCE INOSITOL PHOSPHATE PRODUCTION IN T-CELL RESPONDINGTO MLS(A) SUPERANTIGENS

Previous studies showed that activation of CD4(+) T cells with mouse m ammary tumor virus-encoded Mls(a) superantigens induces strong prolife rative responses and interleukin-2 production but fails to elicit typi cal early T cell receptor (TCR)-mediated signal transduction events, s uch as hydrolysis of polyphosphoinositides (PI) or an increase in intr acellular calcium. Here we show that the failure of Mls(a) antigen to activate PI hydrolysis applies when resting B cells are used as antige n-presenting cells (APC). By contrast, when Mls(a)-bearing B cells are activated for 24h by exposure to lipopolysaccharide or, more importan tly, to Mls(a)-reactive T cells or anti-CD40 antibodies the cells deve lop the capacity to elicit easily detectable PI turnover. These studie s demonstrate that, for B cells as APC, the initiation of certain TCR- associated signal transduction pathways can depend on activation of th e APC. The data suggest that cross talk between T cells and resting B cells can suffice to generate competent B APC and lead to the delayed initiation of signaling pathways important in T cell responses.