IMPAIRED ANTIBODY-RESPONSES IN H-2A(B) MICE

In murine in vivo systems, Ags administered in physiologic solutions t ogether with specific IgE induce a significantly higher Ab response th an Ags administered alone. In vitro, IgE in complex with Ag enhances B cell-mediated presentation of the Ag to T cells. Both phenomena requi re an intact low affinity receptor for IgE (Fc epsilon RII/CD23), sugg esting that the effect on in vivo Ab responses is caused by increased Ag presentation. We here show that mice carrying the MHC class II Ab m olecule (e.g,, C57BL/6 and 129/Sv) do not produce Abs to BSA when immu nized with BSA-2,4,6-trinitrophenyl (TNP) in complex with monoclonal I gE anti-TNP. In contrast, strains of all other MHC haplotypes tested ( H-2(d), H-2(k), H-2(p), H-2(q), and H-2(s)) respond vigorously to IgE/ BSA-TNP complexes, with Ab responses several hundred-fold higher than the responses in H-2(b) mice. C57BL/6 mice were unable to produce a ca rrier-specific response also after immunization with IgE/OVA-TNP, IgE/ diphtheria toxoid-TNP, or IgE/tetanus toxoid-TNP. Although the low res ponsiveness mapped to the Ab region, responsiveness was not restored i n C57BL/6 mice carrying transgenic Ak, suggesting that a nonclassical A-region-encoded gene product is involved. Most importantly, our data call attention to the fact that the C57BL/6 and 129 mouse strains, whi ch are widely used for producing transgenic animals, have defective im mune responses.