In allergic asthmatics, airway inflammation is triggered by specific (inhalation of allergen such as house dust mite allergen and pollen spores) or non-specific triggers (such as air pollutants and viral infection). Most of these inhaled particles are immunologically inert. Dendritic cells (DCs) are essential for priming and T helper-2 differentiation of naïve T cells towards aeroallergens. Contamination of antigens with pattern-associated molecular patterns (PAMPs), such as lipopolysaccharide (LPS), is required to activate DCs to mount an immune response. Damage-associated molecular patterns (DAMPs), such as uric acid and adenosine triphosphate (ATP), also contribute to the induction of inflammation by activation and recruitment of various inflammatory cells. Compelling evidence suggests that a tight collaboration between PAMPs and DAMPs is needed to start an immune response to allergens. Several studies have recently demonstrated an important role of endogenous danger signals at the inception and maintenance phase of allergic disease. Further research into this area should focus on the possible role of these factors in maintenance of chronic disease and induction of airway remodelling.