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The allergic immune response to grass pollen proteins is characterized by the recognition of multiple proteins (allergens) found in grass pollen by the human immune system, typically in genetically predisposed individuals. Upon inhalation, pollen allergens are released rapidly and penetrate mucosal barriers; dendritic cells process and present allergen peptides to T cells, leading to activation and polarization of Th2 helper T cells. Th2 cells secrete cytokines (primarily IL-4, IL-5, and IL-13), fostering IgE production by B cells. IgE binds to the high-affinity receptor (FcεRI) on mast cells and basophils; re-exposure to the same allergens cross-links IgE and triggers cell degranulation, releasing histamine and other mediators, resulting in allergic symptoms. T cell memory responses to previously undescribed grass pollen antigens (not targeted by IgE) also contribute to allergy pathogenesis and represent novel avenues for immunotherapeutic interventions. The allergic response includes both antibody- and T-cell–mediated components, with cross-reactivity to food allergens possible. Immunotherapy strategies target various elements of this response, aiming to induce tolerance or block pathogenic pathways.
Drugs targeting components of the allergic response primarily work by blocking IgE binding to FcεRI, inducing immune tolerance via Treg cells, shifting Th2 to Th1 immune balance, or competing with IgE for allergen binding (via IgG antibodies in immunotherapy).
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