Immune Cell-Mediated Autoimmune Responses in Severe Asthma
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초록
Severe asthma (SA) has heterogeneous inflammatory phenotypes characterized by persistent airway inflammation (eosinophilic and/or neutrophilic inflammation) and remodeling. Various immune cells (eosinophils, neutrophils, and macrophages) become more activated and release inflammatory mediators and extracellular traps, damaging the protective barrier of airway epithelial cells and further activating other immune and structural cells. These cells play a role in autoimmune responses in asthmatic air ways, where the adaptive immune system generates autoantibodies, inducing immunoglobulin G-dependent airway inflamma tion. Recent studies have suggested that adult asthmatics had high titers of autoantibodies associated with asthma severity, al though pathogenic factors or diagnostic criteria are not well-defined. This challenge is further compounded by asthmatics with the autoimmune responses showing therapy insensitivity or failure to current pharmacological and biological treatment. This re view updates emerging mechanisms of autoimmune responses in asthmatic airways and provides insights into their roles, pro posing potential biomarkers and therapeutic targets for SA.
Abstract
Severe asthma (SA) has heterogeneous inflammatory phenotypes characterized by persistent airway inflammation (eosinophilic and/or neutrophilic inflammation) and remodeling. Various immune cells (eosinophils, neutrophils, and macrophages) become more activated and release inflammatory mediators and extracellular traps, damaging the protective barrier of airway epithelial cells and further activating other immune and structural cells. These cells play a role in autoimmune responses in asthmatic air ways, where the adaptive immune system generates autoantibodies, inducing immunoglobulin G-dependent airway inflamma tion. Recent studies have suggested that adult asthmatics had high titers of autoantibodies associated with asthma severity, al though pathogenic factors or diagnostic criteria are not well-defined. This challenge is further compounded by asthmatics with the autoimmune responses showing therapy insensitivity or failure to current pharmacological and biological treatment. This re view updates emerging mechanisms of autoimmune responses in asthmatic airways and provides insights into their roles, pro posing potential biomarkers and therapeutic targets for SA.
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