PREDOMINANT SUPPRESSION OF ANTI-TNP IGE RESPONSE IN MICE BY MONOCLONAL ANTI-TNP IGG1 ANTIBODY - CHARACTERIZATION OF ITS MODE OF ACTION BY IN-VITRO AND IN-VIVO STUDIES

It was found that an antigen-specific IgE response both in vitro and i n vivo was strongly suppressed in the presence of IgG1 monoclonal anti body (mAb) against the antigen. Anti-trinitrophenyl (TNP) IgE response was elicited by the co-culture of C3H B-cells and a conalbumin (CA)-s pecific helper T-cell clone, D10.G4.1, in the presence of 0.1 mu g/ml TNP-CA. Addition of anti-TNP IgG1 monoclonal antibody (mAb) at 1 mu g/ ml to the culture resulted in a marked (>90%) suppression of anti-TNP IgE formation, while anti-TNP IgG1 and IgM responses were affected to a lesser extent (50-60% suppression). Similar observations were made i n in vivo experiments. When 100-200 mu g of anti-TNP IgG1 mAb was inje cted i.p. into BDF1 mice prior to immunization with TNP-CA, the anti-h apten (TNP) IgE response as well as the IgE response to the carrier (C A) was suppressed by 80-90%, while anti-TNP IgM production was inhibit ed by less than 50%. Injection of anti-TNP IgM or IgA mAb showed only marginal effects on anti-TNP IgE production. Spleen cells from anti-TN P IgG1 mAb-treated mice cultured in vitro secreted much lower levels o f anti-TNP IgE spontaneously than those from untreated mice. In in vit ro and in vivo experiments using the F(ab')(2) of anti-TNP IgG1 mAb, a n IgG1 mAb with an irrelevant specificity and mAb directed to Fc gamma RII, it was shown that the binding of the IgG1 mAb with the antigen a nd the interaction of its Fc portion with Fc gamma RII are required fo r the suppressive effects to be exerted.