IgE-mediated suppression of primary antibody responses in vivo.

Abstract

The ability of immunoglobulin (Ig)G to feedback suppress antibody (Ab) responses is a well known property clinically used to prevent haemolytic disease of newborns. We recently found that IgG was able to suppress the primary Ab response to sheep red blood cells (SRBC) in mice lacking the known Fc-receptors for IgG. In addition, IgE and F(ab')2 fragments of IgG were able to suppress the response to SRBC in wild-type mice. These results suggested that the IgG-mediated suppression can take place independently of the IgG (Fc) portion and that masking of the epitopes is an important mechanism. In the present report we investigated whether the suppression caused by IgE is Fc-dependent. Monoclonal IgE anti-2,4,6-trinitrophenyl (TNP), administered with TNP-coupled SRBC (SRBC-TNP), can induce an efficient suppression in mice lacking FcgammaRI + RIII + FcepsilonRI (owing to the lack of the common gamma chain, FcRgamma), FcgammaRIIB or FcepsilonRII (CD23). Because the known IgE-binding receptors are FcepsilonRI, CD23, FcgammaRIIB and FcgammaRIII, the results suggest that also the IgE-mediated suppression can take place independently of the Fc-receptors. A slightly less efficient suppression in CD23-deficient animals, suggests a minor involvement of this receptor.