GENETICS OF ANTIBODIES TO PERIODONTAL PATHOGENS

龋齿和牙周病在某些情况下困扰着大多数人 生命中的时间，是所有年龄段牙齿脱落的主要原因 组。决定抗性或敏感性的因素 这些疾病的致死率都是未知的。这些疾病是由 与牙菌斑相关的微生物，它们在 牙面和牙龈沟。这些生物体的能力 口腔的定植取决于它们对 牙齿表面或其他细菌。特化细胞表面 结构调节细菌在口腔表面的黏附，以及 针对这些结构的抗体已经被证明是 抑制细菌黏附和定植。一个有吸引力的人 对疾病易感性差异的解释是遗传的 粘附性抗体反应的受控变异 牙周病原菌的伴生结构。建议数 项目，该项目基于正在进行的基因控制的研究。 粘性放线菌的血清抗体反应是一种 基因控制血清特异性的详细研究 抗纯化的1型菌毛(T-1)的抗体 粘性放线菌T14V菌株对唾液的粘附性 羟基磷灰石表面。实验将在近交系小鼠身上进行 将使用等电聚焦和独特型特异的酶联免疫吸附试验 确定抗T1抗体的谱型和独特型。 将进行菌株调查，适当的亲本菌株将 被选中进行遗传分析。血清抗T-1抗体 亲本品系、F1杂交小鼠和回交小鼠的反应 将被分析，以及同源基因和 重组近交系小鼠。基因的分离和连锁分析 这些数据将证实这样的假设，即 T-1的血清抗体是由基因决定的，并提供 洞察这种控制的性质。不同的，好吧 特化的抗T-1血清将在体外吸附试验 抑制法检测抗-HBs的谱型和独特型 T1抗体具有抑制A. 粘菌株T14V细胞形成“体外牙面”。这些 研究将有望提供对以下方面的理解： 遗传学在确定疾病易感性和确定 保护性抗T-1抗体反应的特点。这 信息将有助于发展免疫接种。 人类预防或控制牙周病的方案。

Caries and periodontal diseases afflict most individuals at some time during life and are the major causes of tooth loss in all age groups. The factors which determine resistance or susceptibility to these diseases are unknown. These diseases are caused by dental plaque associated microorganisms, which colonize the tooth surface and gingival sulcus. The ability of these organisms to colonize the oral cavity depends upon their adherence to the tooth surface or other bacteria. Specialized cell surface structures mediate the adherence of bacteria to oral surfaces, and antibodies directed against these structures have been shown to inhibit bacterial adherence and colonization. An attractive explanation for differences in disease susceptibility is genetically controlled variations in the antibody response to adherence associated structures on periodontal pathogens. The proposed project, which is based on ongoing studies of genetic control of the serum antibody responses to Actinomyces viscosus, is a detailed study of genetic control of the specificity of serum antibodies to purified type 1 fimbriae (T-1) which mediate the adherence of Actinomyces viscosus strain T14V to saliva coated hydroxyapetite surfaces. Experiments will be done in inbred mice and isoelectric focusing and idiotype specific ELISA's will be used to determine the spectrotypes and idiotypes of anti-T1 antibodies. A strain survey will be done and appropriate parental strains will be selected for genetic analysis. The serum anti-T-1 antibody responses of the parental strains, F1 hybrid and backcross mice will be analyzed, as well as the responses of congenic and recombinant inbred mice. Segregation and linkage analyses of these data will substantiate the hypotheses that the specificity of serum antibodies to T-1 are genetically determined and provide insight into the nature of this control. Different, well characterized anti-T-1 sera will be tested in an in vitro adsorption inhibition assay to correlate the spectrotype and idiotype of anti- T1 antibodies with their ability to inhibit the adherence of A. viscosus strain T14V cells to an "in vitro tooth surface." These studies will hopefully provide an understanding of the role of genetics in determining disease susceptibility and determine the characterisitcs of protective anti-T-1 antibody responses. This information would be useful in the development of immunization protocols in humans to prevent or control periodontal diseases.