| Project/Area Number |
12672033
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Periodontal dentistry
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| Research Institution | NIIGATA UNIVERSITY |
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Principal Investigator |
KOBAYASHI Tetsuo (2002) NIIGATA UNIVERSITY Dental Hospital Lecturer, 歯学部附属病院, 講師 (00215344)
杉田 典子 (2000-2001) 新潟大学, 大学院・歯学部総合研究科, 助手 (30313547)
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| Co-Investigator(Kenkyū-buntansha) |
SUGITA Noriko Graduate School of Medical and Dental Sciences Assistant, 大学院・医歯学総合研究科, 助手 (30313547)
小林 哲夫 新潟大学, 歯学部・総合研究科, 講師 (00215344)
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| Project Period (FY) |
2000 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2002: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2001: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2000: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | Inhibitory receptor / FcγRIIB / Immunoglobulin receptor / Periodontitis susceptibility / Genetic polymorphism / Single nucleotide substitution / Direct sequencing / Polymerase chain reaction / Fc受容体 / 抑制性シグナル / FcγRIIB / B細胞 / 歯周炎 / イムノグロブリン様レセプター / 1塩基多型 |
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| Research Abstract |
FcγRIIB as an immunoregulator :
The inhibitory IgG receptor, FcγRIIB was genetically examined to clarify its role as an immunoregulator. FcγRIIB nucleotide sequence was screened on genomic DNA isolated from peripheral blood of 100 healthy donors with informed consent by means of direct sequencing. We identified 5 and 2 single nucleotide substitutions in exon 4 and intron 4, respectively. Of these, 3 substitutions indicated amino acid changes, which might correspond to the potential splicing sites. However, no change of splicing in the FcγRIIB transcripts was identified with the determination of cDNA sequence. These substitutions located in the extracellular IgG binding domain might induce the structural change of FcγRIIB.
FcγRIIB as a relevant factor for periodontitis susceptibility
We have determined FcγRIIB genotypes for the exon 4 and intron 4, as well as exon 5 bi-allelic polymorphisms in 33 aggressive periodontitis (AGP) patients, 73 chronic periodontitis (CP) patients, and 71 healthy controls, with informed consent, by means of direct sequencing or polymerase chain reaction. Our results indicated a significant over-representation of the nt 775 C allele in the AGP group compared with the control group (AGP vs. Control : 17% vs. 6% ; P=0.01, Odds ratio 3.4), suggesting FcγRIIB gene to be a candidate factor associated with susceptibility to periodontitis.
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