Key mediators in the immunopathogenesis of allergic asthma

• Asthma involves all T-helper subsets with pro and anti-inflammatory properties.
• Innate immunity profoundly shapes the development of asthma.
• ILCs and NKT-cells contribute to the heterogeneity of allergic inflammation.
• Interaction between immune and structural cells dictates chronicity of asthma.
• Potential targets for therapeutic interventions are highlighted.

Asthma is described as a chronic inflammatory disorder of the conducting airways. It is characterized by reversible airway obstruction, eosinophil and Th2 infiltration, airway hyper-responsiveness and airway remodeling. Our findings to date have largely been dependent on work done using animal models, which have been instrumental in broadening our understanding of the mechanism of the disease. However, using animals to model a uniquely human disease is not without its drawbacks. This review aims to examine some of the key mediators and cells of allergic asthma learned from animal models and shed some light on emerging mediators in the pathogenesis allergic airway inflammation in acute and chronic asthma.