## 1 Introduction  
The prevalence of allergic diseases is increasing worldwide, affecting approximately 10-30% of the global population [1]. Allergic diseases result from immune system dysfunction and encompass conditions such as atopic dermatitis (AD), allergic asthma (AAS), allergic rhinitis (AR), and food allergies (FAs). For example, the annual prevalence of atopic diseases is 1.2% in adults in Asia and 17.1% in Europe, while the prevalence among children in Asia ranges from 0.96% to 22.6% [2]. In Japan, the prevalence of allergic diseases among adolescents and adults (ages 18-50) is as follows: AD 15.6%, AAS 14.7%, AR 47.4%, and FAs 12.3%, with AR being the most common [3]. In South Korea, the prevalence of allergic diseases in children is as follows: for infants (\(>\)2 years old), AD, AAS, and AR are 9.0%, 0.9%, and 5.9%, respectively; for preschool children (2-5 years old), 20.2%, 2.3%, and 11.3%; and for school-age children (6-18 years old), 27.6%, 4.1%, and 14.6%. In adults, the prevalence is 17.1%, 3.9%, and 2.3%, respectively, with lower rates observed in the elderly (6.9%, 4.1%, 1.6%) [4]. Allergic diseases manifest in various parts of the body, leading to diverse clinical symptoms [5]. AD is caused by skin barrier dysfunction, abnormal skin microbiota, and localized Th2 immune responses, leading to symptoms such as itching, dryness, and skin lesions [6]. AR and AAS are triggered by allergens, such as airborne molds and pollen. ARleads to symptoms like itching, rhinorrhea, mucus secretion, and smooth muscle contraction in the airways, while AAS results in breathing difficulties, wheezing, chest tightness, and coughing [7]. FAs result from hypersensitivity to specific food allergens and can lead to symptoms such as hypotension, shock, and gastrointestinal reactions [8]. Therefore, new methods are urgently needed to prevent and treat allergic diseases. Most cells, present in the skin and mucosal tissues, are the main cells involved in type 1 allergic diseases [9]. IgE-dependent degranulation promotes the production and secretion of mediators such as histamine, cysteinyl leukotrienes (LTC4, LTD4), prostaglandandins (PGD2, PGI2), cytokines (e.g., IL-4, IL-13), and chemokines, all of which are major contributors to allergic inflammation [10]. For example, histamine is released in the early stages of the allergic response through degranulation, causing vasodilation and increased vascular permeability [11]. Cytokines, through the activation of mast cells and basophils, amplify the inflammatory response [12]. Cysteinyl leukotrienes promote bronchoconstriction, mucus secretion, and immune cell activation, while prostaglandandins contribute to vasodilation. Both of these factors attract neutrophils, stimulating the late-phase allergic response [13; 14]. Mast cell degranulation is mediated by the IgE-dependent high-affinity IgE receptor (FczRI) [15]. When IgE bound to FczRI of mast cells cross-links with a specific antigen (allergen), it induces the release of various chemical mediators (e.g., histamine, \(\beta\)-hexosaminidase, and prostaglandandins) and inflammatory cytokines (e.g., TNF-\(\alpha\) and IL-13), leading to the activation and degranulation of mast cells [16; 17]. FczRI is a heterotetrameric receptor composed of a homodimer of an \(\alpha\) subunit to which IgE binds and \(\beta\) and \(\gamma\) subunits containing an immunoreceptor tyrosine-based activation motif (ITAM) [15]. In humans, FczRI exists in both a tetrameric form (\(\alpha\beta\gamma 2\)) and a trimeric form (\(\alpha\gamma 2\)), whereas in rodents, only the tetrameric form is present [18]. Upon allergen stimulation, FczRI aggregation activates Src family kinases, including Lyn, Fyn, and Syk. Following the binding of the antigen-IgE complex to the \(\alpha\) subunit, Lyn phosphorylates tyrosine residues within the ITAMs of the \(\beta\) and \(\gamma\) subunits, creating docking sites for Syk [19; 20].