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The immune response to house dust mite (HDM) allergens is a complex inflammatory cascade initiated by the inhalation of proteins from mites such as Dermatophagoides pteronyssinus and Dermatophagoides farinae. This process is characterized by the activation of the innate immune system through pattern recognition receptors, such as TLR4, on airway epithelial cells and dendritic cells, which subsequently drive a Th2-polarized adaptive immune response (Hammad & Lambrecht, 2015, Immunity). Key molecular players include cytokines such as IL-4, IL-5, and IL-13, and the production of allergen-specific IgE antibodies that sensitize mast cells and basophils (Galli et al., 2008, Nature). Upon re-exposure, allergen cross-linking of IgE triggers the release of histamine, leukotrienes, and proteases, leading to the clinical manifestations of allergic asthma, rhinitis, and atopic dermatitis. Therapeutic management involves the use of corticosteroids to suppress inflammation, monoclonal antibodies like Omalizumab (anti-IgE) or Dupilumab (anti-IL-4Rα) to block specific signaling pathways, and allergen-specific immunotherapy (AIT) to induce long-term immunological tolerance (Calderon et al., 2015, JACI).
Therapeutic strategies include allergen-specific immunotherapy (AIT) to induce peripheral T-cell tolerance and increase regulatory T-cells (Tregs), and monoclonal antibodies that neutralize IgE or block Th2 cytokine signaling (IL-4, IL-5, IL-13, TSLP) to prevent inflammatory cell recruitment and activation.
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