Immune system response to house dust mite allergens (HDM response)

The immune system response to house dust mite (HDM) allergens is a complex Type I hypersensitivity process primarily driven by the inhalation of proteins from Dermatophagoides species (Jacquet, 2013). Key allergens like Der p 1 and Der p 2 act as primary triggers; Der p 1 is a cysteine protease that disrupts airway epithelial barriers, while Der p 2 mimics MD-2 to facilitate Toll-like receptor 4 (TLR4) signaling (Trompette et al., 2009). This cascade leads to the activation of Th2 cells and the subsequent secretion of pro-inflammatory cytokines such as IL-4, IL-5, and IL-13 (Galli et al., 2008). These cytokines promote B-cell class switching to IgE, which sensitizes mast cells and basophils for immediate-phase reactions upon re-exposure. Therapeutic strategies include neutralizing IgE with omalizumab, blocking cytokine signaling with dupilumab, or inducing desensitization through allergen-specific immunotherapy like Odactra (FDA, 2017). This response is a central driver of chronic conditions including allergic asthma, rhinitis, and atopic dermatitis.

Other names

House dust mite allergyHDM hypersensitivityDermatophagoides pteronyssinus allergyDermatophagoides farinae allergyHDM-induced allergic inflammation

Therapeutic mechanisms include the neutralization of circulating IgE (omalizumab), blockade of the IL-4/IL-13 receptor alpha subunit (dupilumab), inhibition of IL-5 signaling to reduce eosinophils (mepolizumab), and the induction of peripheral T-cell tolerance through allergen-specific immunotherapy (Odactra) (Bousquet et al., 2008; FDA, 2017).