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Alt a 1 is the primary allergen produced by the fungus Alternaria alternata, a ubiquitous mold and significant source of aeroallergens worldwide [1, 5]. Structurally, it is a unique 30 kDa homodimeric glycoprotein characterized by a β-barrel fold, a motif found exclusively in fungi [3, 6]. Biologically, Alt a 1 serves as a fungal effector that facilitates plant infection by transporting flavonoid ligands that neutralize plant defense mechanisms, such as free radicals and pathogenesis-related proteins [1, 4]. In humans, it is the major sensitizing agent for over 80% of Alternaria-sensitive individuals and is strongly associated with the development, persistence, and severity of allergic rhinitis and asthma [3, 13]. As a therapeutic target, Alt a 1 is the central component of molecular allergen-specific immunotherapy (AIT) [11, 16]. This treatment involves the administration of purified natural, recombinant, or polymerized (allergoid) forms of the protein to desensitize the patient's immune system [10, 12]. The mechanism of action involves inducing immune tolerance by shifting the T-cell response from a pro-inflammatory Th2 profile to a regulatory Treg/Th1 profile, which increases the production of blocking IgG4 antibodies and reduces IgE-mediated hypersensitivity [9, 13]. Clinical use of Alt a 1-based therapies has demonstrated efficacy in reducing respiratory symptoms and medication requirements, although safety monitoring for systemic allergic reactions remains a priority during treatment [10, 16].
Allergen-specific immunotherapy (AIT) using Alt a 1 induces immune tolerance by shifting the T-cell response from a pro-inflammatory Th2 profile to a regulatory Treg/Th1 profile, increasing the production of blocking IgG4 antibodies, and reducing IgE-mediated mast cell degranulation.
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