Cross talk between T and B cells generates B antigen-presenting cells able to induce inositol phosphate production in T cells responding to MIsa superantigens

Previous studies showed that activation of CD4⁺ T cells with mouse mammary tumor virus-encoded Mls^a superantigens induces strong proliferative responses and interleukin-2 production but fails to elicit typical early T cell receptor (TCR)-mediated signal transduction events, such as hydrolysis of polyphosphoinositides (PI) or an increase in intracellular calcium. Here we show that the failure of MIs^a antigen to activate PI hydrolysis applies when resting B cells are used as antigen-presenting cells (APC). By contrast, when MIs^a-bearing B cells are activated for 24h by exposure to lipopolysaccharide or, more importantly, to Mls^a-reactive T cells or anti-CD40 antibodies the cells develop the capacity to elicit easily detectable PI turnover. These studies demonstrate that, for B cells as APC, the initiation of certain TCR-associated signal transduction pathways can depend on activation of the 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.