Sell Stewart
Wadsworth Center, New York State Department of Health, Empire State Plaza, Albany, NY, 12201; Albany College of Pharmacy and Health Sciences, 106 New Scotland Avenue Albany, NY, 12208; Division of Biological Sciences, University at Albany, 1400 Washington Avenue, Albany, NY, 12222.
For Immunopathol Dis Therap. 2016;7(3-4):225-236. doi: 10.1615/ForumImmunDisTher.2017020136.
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, , 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.
20世纪60年代免疫病理反应分类的引入,在理解免疫效应机制以及免疫病理疾病的病变如何发展方面带来了重大进展。本文介绍了梅毒、流感和哮喘实验模型的免疫病理机制。梅毒的硬下疳是一种迟发型超敏皮肤反应,由致敏T细胞引发,致敏T细胞激活巨噬细胞以吞噬并杀死间质组织中的感染生物体。实验性流感的主要免疫效应机制是T细胞介导的细胞毒性,其以类似于病毒疹的方式杀死受感染的上皮细胞、支气管内衬细胞和II型肺细胞。小鼠哮喘实验模型的支气管病变之前存在免疫复合物血管炎,而非免疫球蛋白E介导的肥大细胞机制。