It was found that an antigen-specific IgE response both in vitro and in vivo was strongly suppressed in the presence of IgG1 monoclonal antibody (mAb) against the antigen. Anti-trinitrophenyl (TNP) IgE response was elicited by the co-culture of C3H B-cells and a conalbumin (CA)-specific helper T-cell clone, D10.G4.1, in the presence of 0.1 μg/ml TNP-CA. Addition of anti-TNP IgG1 monoclonal antibody (mAb) at 1 μg/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 in in vivo experiments. When 100 - 200 μg of anti-TNP IgG1 mAb was injected i.p. into BDF1 mice prior to immunization with TNP-CA, the anti-hapten (TNP) IgE response as well as the IgE response to the carrier (CA) was suppressed by 80 - 90%, while anti-TNP IgM production was inhibited 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-TNP IgG1 mAb-treated mice cultured in vitro secreted much lower levels of anti-TNP IgE spontaneously than those from untreated mice. In in vitro and in vivo experiments using the F(ab′)2 of anti-TNP IgG1 mAb, an IgG1 mAb with an irrelevant specificity and mAb directed to Fcγ RII, it was shown that the inding of the IgG1 mAb with the antigen and the interaction of its Fc portion with Fcγ RII are required for the suppressive effects to be exerted.
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