FcγRIIB gene polymorphisms in Japanese periodontitis patients

Abstract

Human type II low-affinity receptor for immunoglobulin G (FcgRII) constitutes a clustered gene family consisting of FcgRIIA, IIB and IIC genes. FcgRIIB is unique in its ability to transmit inhibitory signals in B cells via immunoreceptor tyrosine-based inhibitory motif (ITIM). B-cell activation and subsequent elevated production of IgG are the immunopathological features of inflammatory disease such as periodontitis. To determine whether an association with periodontitis susceptibility exists, genetic polymorphisms of FcgRIIB were examined in Japanese patients with aggressive periodontitis (AGP) and chronic periodontitis (CP), and in the race-matched healthy controls (HCs). A significant difference was observed in the distribution of FcgRIIBÀ232I/T allele (exon 5) between the AGP and HC groups, with enrichment of the 232T in the AGP group (P¼0.006). In addition, the FcgRIIB-nt 646À184A/G allele (intron 4) distribution was significantly different between the CP and HC groups, with enrichment of the nt 646À184A in the CP group (P¼0.011). These results document the association of FcgRIIB gene polymorphisms with susceptibility to periodontitis in the Japanese.

The Combined Genotypes of Stimulatory and Inhibitory Fcγ Receptors Associated With Systemic Lupus Erythematosus and Periodontitis in Japanese Adults

“…In this study, we demonstrated an overrepresentation of FcγRIIB‐232T allele in patients with SLE, periodontitis, and both diseases compared to healthy controls. FcγRIIB‐232I/T polymorphism was associated with susceptibility to SLE 16 or aggressive periodontitis 17 in Japanese patients. Our results failed to indicate a significant difference in the FcγRIIB‐232T frequency between SLE patients with and without periodontitis.…”

“…FcγRIIB‐232I/232T genotypes were determined by a combination of PCR and DNA sequencing, as described previously 17 . Briefly, FcγRIIB‐specific PCR was performed in a 2‐‐μl reaction mixture containing 50 ng genomic DNA, 0.5 U Taq polymerase, and FcγRIIB‐specific forward primer (5′‐GGG AAG TAT CGC TGT GAG TTG C‐3′) and reverse primer (5′‐ AGG ATG GAC TTT GGT TAG TGT CTG A‐3′).…”

“…We demonstrated that the stimulatory FcγRIIA‐R131 allele was related to periodontitis risk in SLE patients 15 . It also was shown that the inhibitory FcγRIIB polymorphism (Ile to Thr substitutions at amino acid position 232; 232I/T) was associated with susceptibility to SLE and aggressive periodontitis 16,17 . These results prompted us to investigate whether a combination of stimulatory and inhibitory FcγR genes could elucidate the genetic relevance of both diseases.…”

Genetic polymorphisms and periodontitis

“…Recent case-control studies of our group [7][8][9][10][11][12][13][14][15][16] in Japanese population are summarized in Table 2 and Fig. 1.…”

Caracterización de una muestra de pacientes chilenos con periodontitis y frecuencia del polimorfismo H131R en el receptor FcγRIIa.

“…Es sabido que una dificultad para comparar los distintos estudios es la falta de consenso y homogeneidad de criterios, al usarse diferentes definiciones de periodontitis, las que incluyen: periodontitis crónica, estatus periodontal, enfermedad periodontal, periodontitis del adulto, pacientes con periodontitis, enfermedad periodontal refractaria, periodontitis juvenil localizada, periodontitis agresiva localizada/generalizada, además de pacientes resistentes a periodontitis, a lo que se suma el uso de distintas definiciones de umbral diagnóstico o la ausencia de una definición clara de éste. (14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26) . Por lo mismo, hay coincidencia en que el umbral diagnós-tico, debe ser "preciso, consistente y relativamente precoz en la historia natural de la enfermedad" (1,2) .…”