title: Lower antibody response to Porphyromonas gingivalis associated with immunoglobulin G Fcgamma receptor IIB polymorphism.
abstract: OBJECTIVE
  Human FcgammaRIIB 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 FcgammaRIIB is essential for the negative regulation of antibody production. Our previous study has demonstrated the gene polymorphism FcgammaRIIB-I232T to be associated with periodontitis. The polymorphism FcgammaRIIB-232T has been reported to inhibit B-cell antigen receptor signaling more effectively compared to FcgammaRIIB-232I, while other groups concluded that FcgammaRIIB-232T had no ability to inhibit activatory receptors. In this study, we examined whether FcgammaRIIB-I232T polymorphism would change the IgG antibody response to the periodontopathic bacteria Porphyromonas gingivalis.
  
  
  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 FcgammaRIIB-232T carriers and non-carriers. The FcgammaRIIB-232T carriers revealed a significantly lower IgG(2) response to P. gingivalis 40 kDa OMP compared to non-carriers (p = 0.04, Mann-Whitney U-test). Lower responses of FcgammaRIIB-232T carriers were also observed in specific IgG and IgG(1) levels. The FcgammaRIIB-232T carriers revealed a low level of IgG(2) response to P. gingivalis 40 kDa OMP, even with a high average probing pocket depth.
  
  
  CONCLUSIONS
  These results suggest that association of the FcgammaRIIB-232T allele with periodontitis might be related to the lower levels of antibody response to P. gingivalis.
authors.affiliation: Division of Periodontology, Department of Oral Biological Science, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Honma
authors.forename: N
authors.initials: N
authors.lastname: Sugita
authors.forename: T
authors.initials: T
authors.lastname: Kobayashi
authors.forename: Y
authors.initials: Y
authors.lastname: Abiko
authors.forename: H
authors.initials: H
authors.lastname: Yoshie
mesh_terms: D000328:Adult; D000483:Alleles; D000907:Antibodies, Bacterial / Q000096:biosynthesis* / Q000097:blood; D000917:Antibody Formation; D001425:Bacterial Outer Membrane Proteins / Q000276:immunology; D055113:Chronic Periodontitis / Q000235:genetics / Q000276:immunology*; D005260:Female; D005838:Genotype; D006579:Heterozygote; D006801:Humans; D007074:Immunoglobulin G / Q000096:biosynthesis / Q000097:blood; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D016966:Porphyromonas gingivalis / Q000276:immunology*; D017452:Receptors, IgG / Q000235:genetics* / Q000276:immunology*; D018709:Statistics, Nonparametric; D037521:Virulence Factors / Q000276:immunology
chemical_list: D000907:Antibodies, Bacterial; D001425:Bacterial Outer Membrane Proteins; C499173:FCGR2B protein, human; D007074:Immunoglobulin G; D017452:Receptors, IgG; D037521:Virulence Factors