Prostaglandin E2 as a selective stimulator of antigen-specific IgE response in murine lymphocytes.

Anti-2,4,6-trinitrophenyl (TNP) IgE antibody response was elicited by stimulating TNP-keyhole limpet hemocyanin-primed murine spleen cells with the same antigen in vitro. The released anti-TNP IgE was assayed by antigen- and isotype-specific enzyme immunoassay developed in our laboratory. When prostaglandin E2 (PGE2) was added to the lymphocyte culture at 10(-7) M, anti-TNP IgE response was augmented two- to fourfold. Interestingly, PGE2 did not affect the production of anti-TNP antibodies belonging to other isotypes including IgM, IgG1, IgG2a, IgG2b, IgG3 and IgA. Moreover, PGE2 showed neither enhancing nor interleukin 4-replacing activities in the polyclonal IgE response by B cells stimulated with lipopolysaccharide and interleukin 4. When endogenous prostaglandin synthesis was inhibited by 10(-6) M indomethacin, the anti-TNP IgE response, but not the corresponding IgG response, was suppressed by 30%-60%. These results suggest a potential role of PGE2 in the up-regulation of the antigen-specific IgE response.