Immunopathology of Experimental Models of Syphilis, Influenza, and Asthma.
Immunopathology of Experimental Models of Syphilis, Influenza, and Asthma.
复制标题
DOI：
10.1615/forumimmundisther.2017020136
复制
发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Sell S
中科院分区：
文献类型：
--
作者：
Sell S
20世纪60年代免疫病理学反应分类的引入导致了对免疫效应机制和免疫病理学疾病病变如何发展的理解的重大进展。在这篇文章中，免疫病理机制的实验模型梅毒，流感和哮喘。梅毒下疳是一种迟发性超敏皮肤反应，由致敏T细胞启动，致敏T细胞激活巨噬细胞吞噬并杀死间质组织中的感染生物体梅毒螺旋体。实验性流感中的主要免疫效应机制是T细胞介导的细胞毒性，其以类似于病毒外排的方式杀死感染的上皮细胞、支气管衬里细胞和II型肺细胞。小鼠哮喘实验模型的支气管病变之前是免疫复合物血管炎，而不是免疫球蛋白E介导的肥大细胞机制。
The introduction of immunopathologic reaction classification in the 1960s led to a major advance in understanding immune effector mechanisms and how lesions of immunopathologic diseases developed. In this article, immunopathologic mechanisms are presented for experimental models of syphilis, influenza, and asthma. The chancre of syphilis is a delayed hypersensitivity skin reaction that is initiated by sensitized T cells that activate macrophages to phagocytose and kill the infecting organism, Treponema pallidum, in interstitial tissues. The primary immune effector mechanism in experimental influenza is T-cell–mediated cytotoxicity that kills infected epithelial cells, bronchial lining cells, and Type-II pneumocytes, in a manner similar to viral exanthema. The bronchial lesions of the experimental model of asthma in mice are preceded by an immune complex vasculitis and not an immunoglobulin E–mediated mast cell mechanism.