Adaptive immunity of airway inflammation in asthma

Abstract

Respiratory immunity is responsible for pathogen elimination and prevention of chronic inflammation through both innate and adaptive mechanisms. Inappropriate activation of these immune systems in the respiratory mucosa results in chronic inflammatory airways disease such as asthma. Adaptive immunity is stimulated for example by allergen exposure that activates T and B lymphocytes leading to IgE production and influx of eosinophilic granulocytes into the airways. Presence of IgE and eosinophilia are diagnostic hallmarks as well as key pathogenic components that have been utilized in the search for improved therapies of allergic asthma for the past several decades. The recent breakthroughs in successful clinical application of biologicals in asthma were driven by improved genetic, biochemical, and immunological screening methods, novel imaging and bioinformatics technology, biomarker discovery and a better understanding of immune regulation of allergic airway inflammation. In this chapter we discuss our current understanding of immune regulation of airway inflammation in asthma, with a special focus on the interactions between the adaptive and innate immune systems and the epithelial mucosal tissue.