RHEUMATOID FACTOR--GENETICS, PATHOGENESIS AND MODULATION

类风湿因子——遗传学、发病机制和调节

• 批准号: 6118029
• 负责人: DENNIS A CARSON
• 金额: $ 1.46万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN DIEGO
• 依托单位国家: 美国
• 财政年份: 1998
• 资助国家: 美国
• 起止时间: 1998-12-01 至 1999-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6118029
• 关键词: Escherichia coli; T lymphocyte; antibody specificity; bacterial proteins; blood chemistry; clinical research; gene expression; genetic mapping; human subject; immunopathology; pathologic process; rheumatoid arthritis; synovial fluid

Determine the role of molecular mimicry in the immunopathogenesis of rheumatoid arthritis by comparing the magnitude and specificity of antibodies to the e-coli DNAJ and proteins in the synovial fluid and blood of patients with early RA and normal subjects. Assess the magnitude and specificity of the t-cell immune response to e-coli DNAJ proteins and determine what t-cell receptor variable region genes are used for anti-DNAJ immune responses in RA synovial fluid and blood.

通过比较早期RA患者和正常受试者滑液和血液中大肠杆菌DNAJ和蛋白质抗体的大小和特异性，确定分子模拟在类风湿关节炎免疫发病机制中的作用。 评估T细胞对大肠杆菌DNAJ蛋白免疫应答的程度和特异性，并确定RA滑液和血液中哪些T细胞受体可变区基因用于抗DNAJ免疫应答。