Project/Area Number |
07457461
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Conservative dentistry
|
Research Institution | Kagoshima University |
Principal Investigator |
NAGAOKA Shigetaka Kagoshima Univ., Dental Sch., Associate Professor, 歯学部, 助教授 (10155913)
|
Co-Investigator(Kenkyū-buntansha) |
KITANO Motoo Kagoshima Univ., Dental Sch., Professor, 歯学部, 教授 (10142118)
MATSUSHITA Kenji Kagoshima Univ., Dental Sch., Research Associate, 歯学部, 助手 (90253898)
|
Project Period (FY) |
1995 – 1996
|
Project Status |
Completed (Fiscal Year 1996)
|
Budget Amount *help |
¥7,600,000 (Direct Cost: ¥7,600,000)
Fiscal Year 1996: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1995: ¥5,800,000 (Direct Cost: ¥5,800,000)
|
Keywords | S.mitis / super antigen / periodontitis |
Research Abstract |
Viridans and non-hemolytic streptococci in oral cavity have been suggested to be involved in the occurrence of some oral disorders. However, little is known about the pathogenic roles of extracellular products of these streptococci. Recently, we prepared a superantigenic fraction F-2 from the culture supernatant of Streptococcus mitis 108 isolated from the tooth surface. In this study, we examined the cytotoxic effects of human peripheral blood T cells activated with the F-2 on oral epithelial cells. T cells activated with F-2 exhibited definite cytotoxic effects against the human squamous carcinma HO-1-N-1 cells derived from the oral mucosa and this cyytotoxic effect was increased in a dose-dependent manner by sddition of F-2. Pretreatment with interferon gamma increased the susceptibility of the HO-1-N-1 cells to the cytotoxic effects of F-2-activated cells. No cytotoxic effects were observed when the F-2-activated T cells were separated from the HO-1-N-1 cells. Furthermore, supernatants of the cocultures of target and effect or cells exhibited no cytotoxic effects on HO-1-N-1 cells. The cytotoxicity of the F-2-activated T cells against HO-1-N-1 cells was markedly inhibited by monoclonal antibodies (MAbs) CD11alpha, although T cell proliferation with F-2 was weakly inhibited by this MAbs. On the other hand, the cytotoxicity was weakly inhibited with MAbs against human leukocyte antigen (HLA)-DR and CD2, whereas the T cell proliferative activity were strongly inhibited by these MAbs. These findings suggest that the F-2-dependent T cell-mediated cytotoxicity occurred in a manner different from T cell proliferation with F-2, and to kill the target cells with F-2-activated T cells, the interaction between lymphocyte-function associated antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM-1) was crucial.
|