Possible pathogenic effect of Streptococcus mitis super antigen on oral epithelial cells

轻症链球菌超抗原对口腔上皮细胞可能的致病作用

基本信息

批准号：
07457461
负责人：
NAGAOKA Shigetaka
金额：
$ 4.86万
依托单位：
Kagoshima University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
1995
资助国家：
日本
起止时间：
1995 至 1996
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-07457461/
关键词：
S.mitis super antigen periodontitis

项目摘要

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.

已经建议口腔中的Viridans和非溶血性链球菌参与某些口腔疾病的发生。然而，对于这些链球菌细胞外产物的致病作用知之甚少。最近，我们从从牙齿表面分离的链球菌108的培养上清液中制备了超基因分数F-2。在这项研究中，我们检查了用F-2激活口腔上皮细胞的人外周血T细胞的细胞毒性作用。用F-2激活的T细胞表现出明确的细胞毒性作用对人类鳞状癌HO-1-N-1细胞衍生自口腔粘膜的细胞，并且通过F-2的SDDITION以剂量依赖性的方式增加了这种垂直毒性作用。用干扰素伽马进行预处理增加了HO-1-N-1细胞对F-2激活细胞的细胞毒性作用的敏感性。当将F-2激活的T细胞与HO-1-N-1细胞分离时，未观察到细胞毒性作用。此外，靶和效应的共培养物的上清液或细胞对HO-1-N-1细胞没有细胞毒性作用。单克隆抗体（MABS）CD11Alpha明显抑制了F-2激活的T细胞对HO-1-N-1细胞的细胞毒性，尽管该mAbs弱抑制了T细胞增殖。另一方面，用mAb对人白细胞抗原（HLA）-DR和CD2薄弱地抑制细胞毒性，而这些mABS强烈抑制了T细胞增殖活性。这些发现表明，F-2依赖性T细胞介导的细胞毒性以不同于与F-2的T细胞增殖的方式发生，并用F-2激活的T细胞杀死靶细胞，淋巴细胞功能相关的抗原1（LFA-1）（LFA-1）和细胞间粘附分子-1（ICAM-1）之间的相互作用是cr。