Journal of Clinical and Cellular Immunology
Open Access
ISSN: 2155-9899
+44 1223 790975
ISSN: 2155-9899
+44 1223 790975
Allergic asthma is a chronic inflammatory disease of the lung driven by aberrant responses to normally innocuous environmental allergens. Disease is characterized by excessive IgE synthesis, eosinophilic pulmonary inflammation, mucus hypersecretion, and airway remodeling, and airway hyperresponsiveness - all leading to the clinical features of disease - reversible episodes of coughing, shortness of breath and wheezing. While the excessive production of cytokines like IL-4, IL-5 and IL-13 by allergen specific-Th2 cells is sufficient to explain most features of allergic asthma, increasing evidence suggests that the Th2 paradigm does not explain the full spectrum of disease severity. In particular, severe asthmatics represent a small subset of asthmatics, in which disease is associated with more severe airway reactivity, a mixed eosinophilic/neutrophilic infiltrate, and insensitivity to treatment with corticosteroids. Thus, severe asthmatics are not only more susceptible asthma-related complications; they are underserved by currently available therapies. Recent evidence suggests that the development of severe disease may be associated with the development of a mixed Th2/Th17 response. Herein, we will assess the data from human and animal models suggesting a link between a mixed Th2/Th17 response, and the development of severe asthma. A greater understanding of the mechanisms responsible for the development of severe asthma may allow the development of efficacious therapeutics for the treatment of this intractable form of disease.