Antigen-specific but not polyclonal IgE response in murine B cells cocultured with Th2 clone is refractory to suppression by IL4-depletion.

Abstract

We established culture conditions allowing the induction of antitrinitrophenyl (TNP) IgE response by the coculture of unprimed C3H B cells with conalbumin (CA)-specific type 2 helper T cell clone, D10.G4.1 in the presence of TNP-CA. With the help of this culture system, the role of Th2 cells and interleukin 4 (IL4) derived from them in the induction of antigen-specific IgE response was analyzed. A maximum level of anti-TNP IgE was secreted at 0.5-1 micrograms/ml TNP-CA. When the antigen was increased to 100 micrograms/ml, anti-TNP IgE production was abolished, while antigen-nonspecific (polyclonal) IgE was produced concomitantly. Anti-TNP IgE synthesis was not significantly suppressed in the presence of monoclonal anti-IL4 (11B11), nor was the response further enhanced by the addition of recombinant IL4. In contrast, polyclonal IgE response was abolished by 11B11. In order to deplete endogenous IL4 more strictly, we employed an antisense DNA for IL4 mRNA that can effectively inhibit IL4 production from D10 cells. Even in the presence of both 11B11 and the antisense DNA, it was found that anti-TNP IgE response was not suppressed significantly. These results suggest that antigen-specific IgE response induced in B cells cocultured with established Th2 cells does not depend on IL4 in contrast to polyclonal IgE response.