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Japanese cedar pollen allergens, primarily Cry j 1 and Cry j 2, are the major causative agents of Japanese cedar pollinosis, a highly prevalent seasonal allergic rhinitis in Japan [1, 2, 12]. Cry j 1 is a 41-45 kDa glycoprotein characterized as a pectate lyase, while Cry j 2 is a 37 kDa polygalacturonase; both enzymes are localized within the pollen grain and function to degrade plant cell walls during pollen tube growth [4, 6, 14]. In susceptible individuals, these proteins are recognized by the immune system, leading to the production of allergen-specific IgE antibodies that bind to mast cells and basophils [2, 7]. Upon subsequent exposure, the cross-linking of these antibodies triggers the release of inflammatory mediators, causing symptoms such as sneezing, rhinorrhea, and ocular congestion [9, 13]. Therapeutic strategies primarily focus on allergen-specific immunotherapy (AIT), where standardized extracts of the allergen are administered sublingually or subcutaneously to induce long-term immune tolerance [2, 10, 18]. This desensitization process involves shifting the immune response from a Th2 to a Th1/Treg profile and increasing the levels of protective IgG4 antibodies [9, 11].
Allergen-specific immunotherapy (AIT) induces immune tolerance through the desensitization of T-cells, induction of regulatory T cells (Tregs), and the production of protective allergen-specific IgG4 antibodies which block IgE binding [2, 9, 11, 19].
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