| Project/Area Number |
59440080
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Conservative dentistry
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| Research Institution | Osaka University , Faculty of Dentistry |
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Principal Investigator |
OKADA Hiroshi Osaka Univ., Faculty of Dentistry, Professor, 歯学部, 教授 (40038865)
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| Co-Investigator(Kenkyū-buntansha) |
KASSAI Yasuhiro Osaka Univ., Faculty of Dentistry, instructor, 歯学部, 助手 (60177417)
HARADA Yasushi Osaka Univ., Faculty of Dentistry, instructor, 歯学部附属病院, 助手 (10181025)
KIMURA Shigenobu Osaka Univ., Faculty of Dentistry, assistant Professor, 歯学部附属病院, 講師 (10177917)
FUKUHARA Hironobu Osaka Univ., Faculty of Dentistry, assistant Professor, 歯学部附属病院, 講師 (20144503)
EBISU Shigeyuki Osaka Univ., Faculty of Dentistry, associate Professor, 歯学部, 助教授 (50116000)
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| Project Period (FY) |
1984 – 1986
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| Project Status |
Completed (Fiscal Year 1986)
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| Budget Amount *help |
¥30,500,000 (Direct Cost: ¥30,500,000)
Fiscal Year 1986: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1985: ¥6,000,000 (Direct Cost: ¥6,000,000)
Fiscal Year 1984: ¥23,000,000 (Direct Cost: ¥23,000,000)
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| Keywords | periodontitis / B cell / polyclonal B cell activation / autoreactive T cell / Ia antigen / IgG synthesis / lgG産生 / 自己反応性T細胞 / 自己リンパ球混合培養反応 / 成人型歯周炎患者 / 自己リンパ球混合培養 / Tリンパ球の増殖 / 口腔内細菌 / 多クローン性B細胞活性化 / T細胞依存性IgG産生 |
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| Research Abstract |
Human periodontitis has been confirmed to be IgG producing cell rich lesion. We detected <T4^+> and <T8^+> cells as well as immunoglobulins, particularly IgG, producing cells in periodontal lesions. The incidence of HLA-DR(Ia) was also approximately equal in both <T4^+> and <T8^+> cell population. These results suggested that helper and suppressor functions could participate in the establishment of periodontal lesions.
On the other hand, B cells might be activated polyclonally in periodontal lesion, because a variety of periodontal flora possessed polyclonal B cell activating capacities. We demonstrated that IgG antibody forming cells differentiated from surface IgG positive B cells but not from surface IgG negative B cells. The results suggested that the memory B cells primed with antigens might migrate into periodontal lesions, then they might be activated polyclonally and developed into IgG producing cells.
Periodontal lesion could be, therefore, induced by the collaboration of the immunoregulatory mechanisms by T cells and macrophages with PBA. In fact, T cells, particularly helper/inducer T (Th/i) cells, enhanced IgG synthesis of B cells activated with T-independent B cell activators (TI-PBAs) such as LPS and Actinomyces viscosus preparation. Th/i cells were activated by recognition of Ia expressed on B cells. Ia increased on B cells stimulated with TI-PBAs. Activated Th/i cells produced soluble factors which enhanced IgG synthesis of B cells activated with TI-PBAs. T cells were strongly suggested to participate in the development of periodontal lesions.
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