Artemisia vulgaris major pollen allergen Art v 1 (Art v 1)

Artemisia pollen allergens, specifically the major allergen Art v 1, are the primary drivers of seasonal allergic rhinitis and asthma in regions where mugwort is endemic (PubMed 12421987) [2]. Art v 1 is a defensin-like protein (UniProt Q84ZX5) [3] that triggers Type I hypersensitivity by cross-linking endogenous IgE on mast cells and basophils, leading to the release of inflammatory mediators. The therapeutic target described involves the formation of an immune complex during allergen immunotherapy (AIT), where induced IgG4 and IgA antibodies compete with IgE for allergen binding (MDPI) [4]. This competition, often referred to as blocking activity, prevents the allergen from activating effector cells and modulates T-cell receptor (TCR) signaling to promote immune tolerance (PMC) [5]. Understanding the interaction between these induced antibodies, the allergen, and endogenous receptors is crucial for the development of next-generation allergy vaccines and monitoring treatment efficacy through biomarkers like the IgE/IgG4 ratio [6].

Other names

Mugwort pollen allergen Art v 1Defensin-like protein 1Art v 1.0101Artemisia pollen allergen

Allergen immunotherapy (AIT) induces the production of allergen-specific IgG4 and IgA antibodies, which act as blocking antibodies by competing with endogenous IgE for binding to Artemisia pollen allergens like Art v 1 (MDPI) [4]. This competition prevents the formation of allergen-IgE complexes on mast cells and basophils, thereby inhibiting degranulation and the release of inflammatory mediators. Furthermore, AIT modulates T-cell receptor (TCR) signaling by promoting the differentiation of regulatory T cells (Tregs) and shifting the immune response from a Th2-mediated allergic profile to a Th1 or tolerant profile (PMC) [5].