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Forum on Immunopathological Diseases and Therapeutics
SJR: 0.309 SNIP: 0.041 CiteScore™: 0.18

ISSN Imprimer: 2151-8017
ISSN En ligne: 2151-8025

Archives: Volume 1, 2010 to Volume 7, 2016

Forum on Immunopathological Diseases and Therapeutics

DOI: 10.1615/ForumImmunDisTher.2017020136
pages 225-236

Immunopathology of Experimental Models of Syphilis, Influenza, and Asthma

Stewart Sell
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

RÉSUMÉ

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.


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