TARGETING OF ADCC IN PERIODONTAL DISEASE

这个应用程序的目标是建立一个微生物模型- 靶向抗体依赖细胞介导的细胞毒作用 慢性牙周炎的致病因素 疾病。初步数据显示，多种细菌 制剂能够遵守几种类型的标准 靶细胞，包括人淋巴母细胞系，鸡 绵羊红细胞和人牙龈成纤维细胞。一次 这些细菌是结合在一起的，它们的抗体能够 将ADCC效应器细胞定向到目标，导致 对哺乳动物细胞的破坏。我们建议ADCC“ 靶向“发生在牙周炎中，并导致组织破坏。 因此，在牙周炎的任何阶段，牙龈微生物区系的特征 牙周病的发展，以及菌群结合的能力 对组织来说，会对ADCC的表达产生深远的影响 以及随之而来的组织损伤。我们建议：1)研究 靶向ADCC中的重要因素，包括效应细胞 细菌的亚群、裂解机制和影响 ADCC效应器功能中的准备工作；以及2)检查 牙周病状况与ADCC的关系 检测健康受试者和患者血清中的活性 抗体亲和力、免疫球蛋白亚类和酶联免疫吸附试验的作用 效价。这一模型的特征将提供背景 需要将其确定为发展中的病因 牙周病，并将提供动力，进一步 临床评估，最终目标是 这一机制的药理学控制。

The goal of this application is to establish a model of microbial- targeted antibody-dependent cell-mediated cytotoxicity (ADCC) as an etiologic factor in chronic inflammatory periodontal disease. Preliminary data indicates that a variety of bacterial preparations are capable of adhering to several types of standard target cells, including human lymphoblastoid cell lines, chicken and sheep erythrocytes, and human gingival fibroblasts. Once these bacteria are bound, antibodies to them are capable of directing the ADCC effector cells to the target, resulting the destruction of the mammalian cell. We propose that ADCC " targeting" occurs in periodontitis and results in tissue destruction. Thus, the characteristic gingival microflora at any stage in the development of periodontal disease, and that flora's ability to bind to tissues, will have a profound effect on the expression of ADCC and subsequent tissue damage. We propose to: 1) study the factors important in targeted ADCC, including effector cell subpopulations, lytic mechanisms, and the influence of bacterial preparations in ADCC effector function; and 2) examine the relationship between periodontal disease status and ADCC activity in the sera of healthy subjects and patients by examining the role of antibody affinity, immunoglobulin subclass, and ELISA titer. Characterization of this model will provide the background needed to establish it as an etiologic factor in the development of periodonatal disease and will provide the impetus for further clinical evaluation, with the ultimate goal of possible pharmacologic control of the mechanism.