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*
Department of Immunology, University Hospital Utrecht, Utrecht, The Netherlands;
Bucharest Center of Immunology, Bucharest, Rumania;
Department of Immunology, L. Eötvös University, Budapest, Hungary; and
§
Division of Rheumatology, Washington University School of Medicine, St. Louis, MO 63110
During an ongoing immune response, immune complexes, composed of
Ag, complement factors, and Igs, are formed that can interact with
complement receptors (CRs) and IgG Fc receptors (Fc
R). The role of
CR1/2 and FcR in the regulation of the immune response was
investigated using OVA that was chemically conjugated to whole IgG of
the rat anti-mouse CR1/2 mAb 7G6. FACS analysis using the murine B
cell lymphoma IIA1.6 confirmed that the 7G6-OVA conjugate recognized
CR1/2. Incubating IIA1.6 cells with 7G6-OVA triggered tyrosine
phosphorylation and Ag presentation to OVA-specific T cells in vitro.
Immunizing mice with 7G6-OVA at a minimal dose of 1 µg i.p. per mouse
markedly enhanced the anti-OVA Ig response, which was primarily of
the IgG1 isotype subclass. The 7G6-OVA did not enhance the anti-OVA
response in CR1/2-deficient mice. OVA coupled to an isotype control Ab
induced a considerably lower anti-OVA response compared with that
induced by OVA alone, suggesting inhibition by interaction between the
Fc part of the Ab and the inhibitory FcRIIb on B cells. This finding
was supported by the observation that IIA1.6 cells which were incubated
with 7G6-OVA lost the ability to present Ag upon transfection with
FcRIIb. In sum, 7G6-conjugated OVA, resembling a natural immune
complex, induces an enhanced anti-OVA immune response that involves
at least CR1/2-mediated stimulation and that may be partially
suppressed by FcRIIb.
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