Allergic response is known as an exaggerated reaction of the immune system to harmless environmental substances, such as animal dander, house dust mites, foods, pollen, insects, and chemical agents (Milián and Díaz 2004; Arshad 2010). The initial event responsible for the development of allergic reaction is the generation of allergen-specic CD4+ T helper (Th)2 cells. Once generated, effector Th2 cells produce interleukin (IL)-4, IL-5, IL-9, and IL-13, which cause the production of allergen-specic immunoglobulin E (IgE) by B cells (Akdis, Blaser, and Akdis 2005). Subsequently, allergic reactions are induced upon binding of allergen to IgE, which is tethered to the high-afnity IgE receptor on the surface of mast cells and basophils. After the aggregation of cell-surface receptors is a cascade of intracellular events, including the increase of the intracellular Ca2+ level, the release of preformed inammatory mediators from secretary granules such as histamine and β-hexosaminidase, and the generation and secretion of the newly synthesized substances such as leukotrienes, prostaglandins, and cytokines. These mediators cause allergic inammatory responses due to airway constriction, mucous production, and recruitment of inammatory cells (Galli, Tsai, and Piliponsky 2008). Accordingly, the control of Th2-type cytokine expression, IgE levels, and inammatory mediator production are especially important for the regulation of type I allergic reaction; thus, allergic diseases may be managed. Although successful immune modulation of allergic disease has been demonstrated in vivo, it often fails to translate into human clinical trials (Nguyen and Casale 2011). Thus, the search for potential drug candidates containing higher immunomodulatory activity is increasing in the pharmaceutical industry. In this regard, natural bioactive compounds and their derivatives are great sources for the development of new-generation antiallergic therapeutics.