Immune regulation by the inhibitory IgG receptor related to the susceptibility of periodontitis

人低亲和力Fc受体IIb(FcγRIIb)是免疫球蛋白G受体的一种，通过免疫复合物与B细胞受体(Bcr)交联，抑制B淋巴细胞的活化。FcγRIIb的这一功能对于抗体产生的负调控是必不可少的。我们先前的研究已经证明FcγRIIB-I232T基因多态性与牙周炎显著相关。在这项研究中，我们检测了不同基因型牙周炎患者对牙周病致病细菌牙龈卟啉单胞菌(P.gigivalis)的抗体反应是否存在差异。采用基因组直接测序法对47例牙周炎患者进行Fc-γ基因RIIB-I232T分型。测定了重组40 kDa外膜蛋白(OMP)和200 kDa抗原蛋白(AP)的血清非特异性总免疫球蛋白(TIgM)和牙周炎肺炎衣原体(P.givalis)的特异性免疫球蛋白亚类。FcγRIIB-232T携带者对P.gin…的免疫应答显著降低与非携带者相比，更多的是40 kDa的OMP(P&lt；0.05)。FcγRIIB-232T携带者的特异性Ig G和Ig G1值也较低，但差异无统计学意义。FcγRIIB-232T携带者与非携带者对牙龈假单胞菌和200 kDa AP的抗体应答无显著差异。在FcγRIIB-232T非携带者中，有一组患者表现出高水平的免疫球蛋白G_2应答和高平均探测深度。相反，所有FcγRIIB-232T携带者表现出较低的IgG2应答水平。这些结果提示FcγRIIB-232T等位基因与牙周炎的相关性可能与牙周炎患者对牙周炎的抗体应答水平较低有关。牙周炎患者B淋巴细胞表面Fc、γ、RIIb的表达水平明显低于对照组。这可能是在牙周炎发病机制中抑制B淋巴细胞过度激活效果较差的原因之一。FcγRIIb在牙周炎患者牙周组织中的表达也得到证实。较少

Human low affinity Fc receptor IIb (FcγRIIb) is one of IgG receptors and suppress the activation of B lymphocytes through cross-linking with B cell receptor (BCR) via immune-complexes. This function of FcγRIIb is essential for the negative regulation of antibody productions. Our previous study has demonstrated the gene polymorphism FcγRIIB-I232T to be significantly associated with periodontitis. In this study, we examined the possibility that IgG antibody responses to periodontopathic bacteria Porphyromonas gingivalis (P.gingivalis) are different between periodontitis patients with different genotypes. Forty-seven patients with periodontitis were genotyped for FcγRIIB-I232T with the direct sequencing of genome DNA. Serum levels of nonspecific total IgG and specific IgG subclasses for the sonicate of P.gingivalis, the recombinant 40-kDa outer membrane protein (OMP) and 200kDa antigenic protein (AP) were determined. FcγRIIB-232T carrier revealed significantly lower IgG2 response to P.gin … More givalis 40-kDa OMP compared to noncarrier (P<0.05). Lower responses of FcγRIIB-232T carrier were also observed in specific IgG and IgG1 levels which were not statistically significant. No significant difference of antibody response to P.gingivalis sonicate or 200-kDa AP was observed between FcγRIIB-232T carrier and noncarrier. In FcγRIIB-232T noncarrier, there was a subgroup of patients showing high levels of IgG2 response in concert with the high average of probing depth. In contrast, all FcγRIIB-232T carriers revealed lower levels of IgG2 response. These results suggest that the association of FcγRIIB-232T allele with periodontitis might be attributed to the lower level of antibody response to P.gingivalis.We investigated the expression of FcγRIIb in peripheral blood leukocytes and gingiva from periodontitis patients. Expression levels of FcγRIIb on B lymphocytes were lower in patients with periodontitis compared to controls. This might be a cause of less effective inhibition of overactivation of B lymphocytes in the pathogenesis of periodontitis. Expression of FcγRIIb was also confirmed in human gingiva with periodontitis. Less