Immune response to grass pollen allergens

The immune response to grass pollen allergens is a complex physiological process characterized by a Type I hypersensitivity reaction in sensitized individuals. Upon exposure to proteins from grass pollens, such as those from Timothy grass (Phleum pratense), the immune system produces allergen-specific IgE antibodies that bind to high-affinity receptors on mast cells and basophils (Valenta et al., 2019, PMID: 30633301). Subsequent exposure triggers the cross-linking of these IgE molecules, leading to degranulation and the release of inflammatory mediators like histamine, leukotrienes, and cytokines (StatPearls, 2023, NBK448118). This cascade results in the clinical manifestations of allergic rhinitis, conjunctivitis, and allergic asthma. While not a single molecular target, this response is modulated by various drugs, including H1-antihistamines, leukotriene receptor antagonists, and corticosteroids. Furthermore, allergen-specific immunotherapy (AIT) is used to modify the underlying disease by inducing regulatory T cells and "blocking" IgG4 antibodies, effectively desensitizing the patient to the pollen (Durham & Shamji, 2023, PMID: 36631134). This therapeutic approach aims to shift the immune response from a Th2-dominated allergic profile to a more tolerant Th1 or Treg-mediated state.

Other names

Grass pollen allergyHay feverAllergic rhinitis to grass pollenType I hypersensitivity to PoaceaeGrass pollen-induced allergic response

Drugs targeting this response act through several pathways: H1-antihistamines competitively inhibit histamine at the H1 receptor; corticosteroids suppress the transcription of pro-inflammatory cytokines; omalizumab binds to circulating IgE to prevent its interaction with FceRI; and allergen-specific immunotherapy (AIT) induces immune tolerance by promoting regulatory T cell (Treg) activity and shifting the immune profile from Th2 to Th1 (PMID: 30633301, PMID: 36631134).