HUMAN B-CELLS EXPRESS IL-5 RECEPTOR MESSENGER-RIBONUCLEIC-ACID AND RESPOND TO IL-5 WITH ENHANCED IGM PRODUCTION AFTER MITOGENIC STIMULATIONWITH MORAXELLA-CATARRHALIS

The potential for IL-5 to regulate human B cells is controversial desp ite its well established role as a regulatory factor for murine B cell s, We hypothesized that the mechanism by which human B cells were stim ulated would, as with murine B cells, determine their potential to res pond to IL-5. Since Staphylococcus aureus Cowan strain I (SAG) and Mor axella catarrhalis (MCat) stimulate human B cells by distinct interact ions with cell-surface Ig, we compared their potential to induce an IL -5-responsive state by human B cells purified to homogeneity, Neither SAC alone nor SAC plus IL-5 stimulated Ig production, although microgr am quantities of IgM were produced with SAC plus IL-2. In contrast, MC at induced microgram quantities of IgM by B cells in the absence of ex ogenous cytokines, and IL-5 significantly increased IgM production ove r twofold in the majority of donors. Synergism of IL-5 and IL-2 was de tected using suboptimal concentrations of IL-2 with MCat-, but not SAC -, stimulated B cells, Donor B cells unresponsive to IL-5 when stimula ted with MCat, became IL-5 responsive in the presence of IL-2, Since m essage for the IL-5R alpha, IL-5R beta, and soluble IL-5R alpha chains was detected in freshly isolated B cells, we further investigated whe ther IL-5 responsiveness to MCat, but not SAG, was due to their differ ential regulation of IL-5R mRNA, Surprisingly, stimulation by either M Cat or SAG, without or with IL-2, increased both IL-SR alpha and IL-SR beta mRNA and decreased soluble IL-5R alpha mRNA, These studies demon strate that, as with murine B cells, human B cells express message for IL-5R but can respond to IL-5 only if appropriately stimulated to und ergo terminal differentiation.