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首页> 外文期刊>Journal of Periodontology >The combined genotypes of stimulatory and inhibitory fcgamma receptors associated with systemic lupus erythematosus and periodontitis in Japanese adults.
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The combined genotypes of stimulatory and inhibitory fcgamma receptors associated with systemic lupus erythematosus and periodontitis in Japanese adults.

机译:日本成年人中与系统性红斑狼疮和牙周炎有关的刺激性和抑制性Fcγ受体的联合基因型。

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BACKGROUND: The pathobiology of systemic lupus erythematosus (SLE) is similar to that of periodontitis in that the immunoglobulin G Fc receptor (FcgammaR) and proinflammatory cytokines play an important role. Genetic variations of FcgammaR and interleukin (IL)-1 are associated with susceptibility to both diseases. Therefore, we evaluated whether the combination of FcgammaR or IL-1 polymorphic genes represents a common risk factor for SLE and periodontitis. METHODS: The study population consisted of Japanese adults with SLE and periodontitis (SLE+P group; n = 46), SLE only (SLE group; n = 25), periodontitis only (P group; n = 58), and healthy individuals with no systemic or oral disease (H group; n = 44). Clinical periodontal condition was evaluated by measurement of probing depth, clinical attachment level, and alveolar bone loss. Genomic DNA was isolated from peripheral blood and analyzed for determination of FcgammaR genotypes (FcgammaRIIA, FcgammaRIIB, FcgammaRIIIA, and FcgammaRIIIB) and IL-1 genotypes (IL-1A +4845 and IL-1B +3954) by allele-specific polymerase chain reactions or DNA sequencing. RESULTS: A significant overrepresentation of the R131 allele of stimulatory FcgammaRIIA and the 232T allele of inhibitory FcgammaRIIB was found in the SLE+P group compared to the H group (P = 0.01 and P = 0.0009, respectively). The combination of FcgammaRIIA-R131 and FcgammaRIIB-232T alleles yielded a strong association with SLE and periodontitis (SLE+P group versus P group: P = 0.01, odds ratio: 3.3; SLE+P group versus H group: P = 0.0009, odds ratio: 11.2). Furthermore, SLE patients with the combined FcgammaR risk alleles exhibited more severe periodontal tissue destruction compared to other SLE patients. The frequencies of IL-1 polymorphic alleles were too low to assess the association with SLE or periodontitis. CONCLUSION: The combination of stimulatory FcgammaRIIA and inhibitory FcgammaRIIB genotypes may increase susceptibility to SLE and periodontitis in the Japanese population.
机译:背景:系统性红斑狼疮(SLE)的病理生物学与牙周炎相似,因为免疫球蛋白G Fc受体(FcgammaR)和促炎细胞因子起着重要的作用。 FcγR和白介素(IL)-1的遗传变异与两种疾病的易感性有关。因此,我们评估了FcgammaR或IL-1多态性基因的组合是否代表SLE和牙周炎的常见危险因素。方法:研究人群包括日本成年人SLE和牙周炎(SLE + P组; n = 46),仅SLE(SLE组; n = 25),仅牙周炎(P组; n = 58)和健康个体。无全身或口腔疾病(H组; n = 44)。通过测量探查深度,临床附着水平和牙槽骨丢失来评估临床牙周状况。从外周血中分离出基因组DNA,并通过等位基因特异性聚合酶链反应或DNA测序。结果:与H组相比,在SLE + P组中发现刺激性FcgammaRIIA的R131等位基因和抑制性FcgammaRIIB的232T等位基因显着过量(分别为P = 0.01和P = 0.0009)。 FcgammaRIIA-R131和FcgammaRIIB-232T等位基因的组合与SLE和牙周炎密切相关(SLE + P组与P组:P = 0.01,优势比:3.3; SLE + P组与H组:P = 0.0009,优势比例:11.2)。此外,与其他SLE患者相比,合并了FcgammaR风险等位基因的SLE患者表现出更严重的牙周组织破坏。 IL-1多态性等位基因的频率太低,无法评估与SLE或牙周炎的关联。结论:刺激性FcgammaRIIA基因型和抑制性FcgammaRIIB基因型的组合可能增加日本人群对SLE和牙周炎的敏感性。

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