IgE-mediated suppression of primary antibody responses in vivo

The ability of immunoglobulin (Ig)G to feedback suppress antibody (Ab) resp onses is a well known property clinically used to prevent haemolytic diseas e 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-re ceptors 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 i s Pc-dependent. Monoclonal IgE anti-2,4,6-trinitrophenyl (TNP), administere d with TNP-coupled SRBC (SRBC-TNP), can induce an efficient suppression in mice lacking Fc gamma RI f RIII + Fc epsilon RI towing to the lack of the c ommon gamma chain, FcR gamma), Fc gamma RIIB or Fc epsilon RII (CD23). Beca use the known IgE-binding receptors are Fc epsilon RI, CD23, Fc gamma RIIB and Fc gamma RIII, the results suggest that also the IgE-mediated suppressi on can take place independently of the Fc-receptors. A slightly less effici ent suppression in CD23-deficient animals, suggests a minor involvement of this receptor.