THE ROLE OF TYPE 17 HELPER T LYMPHOCYTES IN LATE-PHASE AIRWAY INFLAMMATION IN PATIENTS WITH ALLERGIC ASTHMA

Abstract

Allergic asthma is a chronic inflammatory disease of the airways. Allergeninduced early-phase asthmatic reaction occurs within minutes after allergen inhalation and is considered a result of immunoglobulin E-mediated mast cell activation and release of various mediators, which induce an acute fall in lung function and symptoms of acute asthma. In part of patients with allergic asthma, early-phase asthmatic reaction is followed by a secondary fall in lung function. This late-phase asthmatic reaction is characterized by the influx of inflammatory cells, which are predominantly eosinophils, as well as neutrophils, basophils, and T cells. The late-phase asthmatic reaction is associated with an increase in airway hyperresponsiveness and leads to airway remodeling, which develops as the disease progresses. The differences between the pathways leading to the isolated early- or late - phase asthmatic reaction have not been known. The study using mouse asthma models has shown that type 17 T helper lymphocytes and their cytokines are involved in antigen-induced neutrophil recruitment. The sputum interleukin-17 levels were found to be higher in patients with asthma and correlated with airway hyperresponsiveness to methacholine and asthma severity. The inhalation of Dermatophagoides pteronyssinus allergen leads to the increased percentage of type 17 T helper lymphocytes and elevated interleukin -17 levels associated with late-phase allergen-induced airway inflammation in allergic asthma.