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*
Department of Genetics and Pathology, Uppsala University Hospital, Uppsala, Sweden;
Department of Immunology, Stockholm University, Stockholm, Sweden; and
Microbiology and Tumorbiology Center, Karolinska Institute, Stockholm, Sweden
In murine in vivo systems, Ags administered in physiologic
solutions together with specific IgE induce a significantly higher Ab
response than Ags administered alone. In vitro, IgE in complex with Ag
enhances B cell-mediated presentation of the Ag to T cells. Both
phenomena require an intact low affinity receptor for IgE
(Fc
RII/CD23), suggesting 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 molecule (e.g., C57BL/6 and 129/Sv) do
not produce Abs to BSA when immunized with BSA-2,4,6-trinitrophenyl
(TNP) in complex with monoclonal IgE anti-TNP. In contrast, strains
of all other MHC haplotypes tested (H-2d, H-2k,
H-2p, H-2q, and H-2s) respond
vigorously to IgE/BSA-TNP complexes, with Ab responses several
hundred-fold higher than the responses in H-2b mice.
C57BL/6 mice were unable to produce a carrier-specific response also
after immunization with IgE/OVA-TNP, IgE/diphtheria toxoid-TNP, or
IgE/tetanus toxoid-TNP. Although the low responsiveness mapped to the
Ab region, responsiveness was not restored in 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,
which are widely used for producing transgenic animals, have defective
immune responses.
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