MOLECULAR IMMUNOPATHOLOGY OF AGING

衰老的分子免疫病理学

• 批准号: 6233976
• 负责人: CURTIS B WILSON
• 金额: $ 10.91万
• 依托单位: SCRIPPS RESEARCH INSTITUTE, THE
• 依托单位国家: 美国
• 财政年份: 1996
• 资助国家: 美国
• 起止时间: 1996-12-01 至 1997-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6233976
• 关键词: RNase protection assay; aging; amyloid proteins; chymotrypsin inhibitor; endopeptidases; extracellular matrix; genetically modified animals; glomerulosclerosis; immunocytochemistry; immunopathology; in situ hybridization; interstitial nephritis; kidney cell; laboratory rabbit; laboratory rat; messenger RNA; molecular pathology; nephrosclerosis; neuritic plaques; nuclear runoff assay; protease inhibitor; stromelysin

In this project the following four areas of investigation are outlined: (1) to assess and quantitate the morphological and functional damage produced in the choroid plexus (CP) by immune complexes (IC) and anti-tissue mechanisms of immunopathologic injury; (2) to evaluate the frequency of CP damage and its relationship to CNS abnormalities in human autoimmune anti-basement membrane antibody disease (ABMAbD), Goodpasture's syndrome; (3) to make an assessment of the factors which render the CP and other vascular beds such as the lung susceptible to direct antibody attack; (4) to evaluate the role of molecular mimicry in establishing autoimmune responses which can damage tissue. These studies will focus on factors which affect vascular permeability and thereby permit antibody accumulation to occur. Age-related factors which may influence the susceptibility to attack will be evaluated since the clinical features of patients with ABMAbD vary with age. This work will involve the development of assays to detect cross-reactions of monoclonal antibodies, particularly anti-viral, with tissue antigens in the antigenically complex basement membrane-containing walls of the glo-merular, alveolar and CP capillaries.

在该项目中，概述了以下四个调查领域：（1） 评估和量化在中产生的形态和功能损害 免疫复合物（IC）和反组织机制的脉络丛（CP） 免疫病理损伤； （2）评估CP损坏的频率和 它与人类自身免疫性抗BASEMENT的中枢神经系统异常的关系 膜抗体疾病（ABMABD），Goodpasture综合征； （3）做一个 评估渲染CP和其他血管床的因素 由于肺部容易受到直接抗体攻击； （4）评估角色 分子模仿在建立自身免疫反应时可能会损害的 组织。 这些研究将集中于影响血管的因素 渗透性，从而允许抗体积累。 与年龄有关 可能会评估可能影响攻击易感性的因素 由于ABMABD患者的临床特征随着年龄的增长而变化。 这 工作将涉及开发测定法以检测交叉反应 单克隆抗体，尤其是抗病毒抗体，含有组织抗原 抗原复杂的地下室膜膜的壁， 牙槽和CP毛细血管。