Allergic rhinitis (AR) is a common inflammatory disease characterized by recurring episodes of sneezing, pruritis, and rhinorrhea. It is associated with other co-morbidities, such as asthma, dermatitis, and sinusitis, and is typically triggered by airborne allergens, such as dust mites, pollen, and pet dander, mediated by IgE antibodies. AR is manifested through the adaptive immune system which, compared to the innate immune system, has more specificity and greater memory capabilities. One of the key components of the adaptive immune system are antigen-presenting cells (APC), including macrophages and dendritic cells, which engulf the allergen and allow it to be recognized by lymphocytes, predominately T cells. Through the production of interleukins (IL), activated T cells interact with B cells, allowing them to undergo terminal differentiation, or class-switching, and begin production of IgE molecules that are specific to the allergen which has been captured. The IgE produced then binds to effector cells, such as basophils and mast cells, which release inflammatory chemicals, predominately histamine, when encountering the same allergen again in the future. Although this process was previously believed to occur in the larger lymphoid structures of the body, it is now understood that it occurs predominately in the upper respiratory mucosal epithelium and locoregional lymph tissue. The early phase of inflammation, after repeat exposure to a previously sensitized allergen, occurs within minutes of exposure and is characterized by the release of pre-formed mediators, while the late phase occurs hours later and is associated with the influx of inflammatory cells, primarily eosinophils.