PATHOGENESIS OF URTICARIA, ANGIOEDEMA AND VASCULITIS

荨麻疹、血管性水肿和血管炎的发病机制

• 批准号: 3105018
• 负责人: ALLEN P KAPLAN
• 金额: $ 19.82万
• 依托单位: STATE UNIVERSITY NEW YORK STONY BROOK
• 依托单位国家: 美国
• 财政年份: 1979
• 资助国家: 美国
• 起止时间: 1979-09-01 至 1987-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3105018
• 关键词: autoantibody; autoimmune disorder; biopsy; cell population study; cellular immunity; delayed hypersensitivity; hereditary angioneurotic edema; histamine release; human subject; immune complex; immunofluorescence technique; immunoglobulin E; inflammation; lymphocyte; prostaglandins; rheumatism; urticaria; vasculitis

Our Center is studying the biochemical and physiologic pathways responsible for the inflammation associated with urticaria, angioedema, urticarial vasculitis and vasculitis associated with autoimmune diseases. We know that cold urticaria is histamine-mediated, and, in some cases IgE-dependent. We hope to determine the mechanism by which IgE leads to mast cell degranulation in this disorder as well as dermatographism and assess the role of acetylcholine release in the pathogenesis of cholinergic urticaria. A possible role for kinins and arachidonic acid metabolites as mediators of cholinergic urticaria will be sought and the role of kinins in causing the swelling seen in hereditary angioedema will be defined. A link between the Hageman factor-kallikrein system and the classical complement cascade will be sought in whole plasma and further studied using purified proteins. We will also examine possible immune and non-immune mechanims responsible for the release of histamine and other vasoactive agents in chronic urticaria and angioedema. Finally, we will examine mechanisms by which inflammation may be modulated in connective tissue diseases and other vasculitides including identification of antigens responsible for immune complex formation, the role of vasoactive factors in immune complex localization and the relationship of disease severity and reticuloendothelial clearance of complexes.

我们的中心正在研究生物化学和生理途径， 荨麻疹、血管性水肿、荨麻疹性血管炎相关炎症 以及与自身免疫性疾病相关的血管炎。 我们知道寒冷性荨麻疹 是组胺介导的，并且在某些情况下是IgE依赖性的。 我们希望能确定 IgE导致肥大细胞脱颗粒的机制 以及皮肤划痕症，并评估乙酰胆碱释放的作用， 胆碱能性荨麻疹的发病机制。 激肽的一个可能的作用， 花生四烯酸代谢物作为胆碱能荨麻疹的介质， 寻求和激肽的作用，在引起肿胀看到遗传性 将定义血管性水肿。 哈格曼因子-激肽释放酶系统 将在整个血浆中寻找经典的补体级联反应， 使用纯化的蛋白质进行研究。 我们还将检查可能的免疫和 非免疫机制负责释放组胺和其他 慢性荨麻疹和血管性水肿中的血管活性剂。 最后，我们将研究 结缔组织疾病中炎症的调节机制 和其他血管炎，包括鉴定负责 免疫复合物的形成，血管活性因子在免疫复合物中的作用 网状内皮细胞的定位及其与疾病严重程度的关系 清除复合物。