Allergic rhinitis a chronic inflammatory disease of the upper airways that has a major impact on the quality of life of patients and is a socio-economic burden. Understanding the underlying immune mechanisms is central to developing better and more targeted
therapies. The inflammatory response in the nasal mucosa includes an immediate
IgE-mediated mast cell response as well as a latephase response characterized by recruitment of eosinophils, basophils, and T cells expressing Th2
cytokines including
interleukin (IL)-4, a switch factor for
IgE synthesis, and
IL-5, an eosinophil
growth factor and on-going allergic
inflammation. Recent advances have suggested new pathways like local synthesis of
IgE, the
IgE-
IgE receptor mast cell cascade in on-going allergic
inflammation and the epithelial expression of
cytokines that regulate Th2
cytokine responses (i.e.,
thymic stromal lymphopoietin, IL-25, and IL-33). In this review, we briefly review the conventional pathways in the pathophysiology of
allergic rhinitis and then elaborate on the recent advances in the pathophysiology of
allergic rhinitis. An improved understanding of the immune mechanisms of
allergic rhinitis can provide a better insight on novel therapeutic targets.