The potential for IL-5 to regulate human B cells is controversial despite its well established role as a regulatory factor for murine 8 cells. We hypothesized that the mechanism by which human B cells were stimulated would, as with murine B cells, determine their potential to respond to IL-5. Since Staphylocoecus aureus Cowan strain I (SAC) and Moraxella catarrhalis (MCat) stimulate human B cells by distinct interactions 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 microgram quantities of IgM were produced with SAC plus IL-2. In contrast, MCat induced microgram quantities of IgM by B cells in the absence of exogenous cytokines, and IL-5 significantly increased IgM production over twofold in the majority of donors. Synergism of IL-5 and IL-2 was detected using suboptimal concentrations of IL-2 with MCat-, but not SAC-, stimulated B cells. Donor B cells unresponsive to IL-5 when stimulated with MCat, became IL-5 responsive in the presence of IL-2. Since message for the IL-SRα, IL-5Rβ, and soluble IL-5Rα chains was detected in freshly isolated B cells, we further investigated whether IL-5 responsiveness to MCat, but not SAC, was due to their differential regulation of IL-5R mRNA. Surprisingly, stimulation by either MCat or SAC, without or with IL-2, increased both IL-SRα and IL-5Rβ mRNA and decreased soluble IL-5Rα mRNA. These studies demonstrate 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 undergo terminal differentiation.
|Original language||English (US)|
|Number of pages||10|
|Journal||Journal of Immunology|
|State||Published - Feb 15 1996|
ASJC Scopus subject areas
- Immunology and Allergy