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Chain-Deficient Mice and Increased in FcRII-Deficient Mice1
Departments of
*
Genetics and Pathology and
Animal Development and Genetics, Uppsala University, Uppsala, Sweden; and
Department of Immunology, University Hospital Utrecht, Utrecht, The Netherlands
Immunization with IgG/Ag or IgE/Ag complexes leads to a higher
production of specific Abs than immunization with Ag alone. The
enhancing effect of IgE is exclusively dependent upon the low-affinity
receptor for IgE, Fc
RII, whereas the mechanism behind IgG-mediated
enhancement is unknown. We have investigated whether receptors for the
Fc part of IgG are required for responses to IgG/Ag. Mice lacking the
subunit of Fc receptors (FcRs) (FcR-/-), FcRII
(FcRII-/-), or FcRIII (FcRIII-/-)
were immunized with BSA-2,4,6-trinitrophenyl (TNP) alone or BSA-TNP
complexed to monoclonal TNP-specific IgG1, IgG2a, or IgG2b. As
expected, all subclasses enhanced the Ab-response to BSA in wild-type
mice. Enhancement was in the same order of magnitude in
FcRIII-/- mice (
177-fold of controls administered Ag
alone), whereas it was abrogated in FcR-/- mice and
augmented in FcRII-/- mice (5147-fold of controls).
The response to IgE/Ag complexes in FcR-/- and
FcRII-/- mice was similar to that seen for wild-type
mice, demonstrating that non-FcR-dependent responses were normal.
Our observations suggest that IgG/Ag complexes enhance Ab responses via
FcRs. Moreover, they reveal a strong negative regulation of Ab
responses to IgG/Ag exerted by FcRII.
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