AbstractBackground and Objective
Human FcγRIIB is one of the receptors for immunoglobulin G (IgG) and suppresses the activation of B lymphocytes through cross-linking with the B cell receptor via immune complexes. This function of FcγRIIB is essential for the negative regulation of antibody production. Our previous study has demonstrated the gene polymorphism FcγRIIB-I232T to be associated with periodontitis. The polymorphism FcγRIIB-232T has been reported to inhibit B-cell antigen receptor signaling more effectively compared to FcγRIIB-232I, while other groups concluded that FcγRIIB-232T had no ability to inhibit activatory receptors. In this study, we examined whether FcγRIIB-I232T polymorphism would change the IgG antibody response to the periodontopathic bacteria Porphyromonas gingivalis.Material and Methods
Forty-seven patients with periodontitis were genotyped with the direct sequencing of genome DNA. Serum IgG and specific IgG subclass levels for the sonicate of P. gingivalis and the recombinant 40 kDa outer membrane protein (OMP) were determined.Results
No significant difference in the total IgG level and IgG response to P. gingivalis sonicate were observed between sera from FcγRIIB-232T carriers and non-carriers. The FcγRIIB-232T carriers revealed a significantly lower IgG2 response to P. gingivalis 40 kDa OMP compared to non-carriers (p=0.04, Mann–Whitney U-test). Lower responses of FcγRIIB-232T carriers were also observed in specific IgG and IgG1 levels. The FcγRIIB-232T carriers revealed a low level of IgG2 response to P. gingivalis 40 kDa OMP, even with a high average probing pocket depth.Conclusion
These results suggest that association of the FcγRIIB-232T allele with periodontitis might be related to the lower levels of antibody response to P. gingivalis.