Fig. 3

Simplified model of the HDM-induced innate immune activation leading to IgE sensitization in the airways. The induction ofTh2 immunity by HDM allergens results from the stimulation of different innate immune pathways. HDM protease allergens specifically cleave protease sensitive receptors including protease-activated receptor (PAR)-2, disrupt epithelial barrier to gain access to dendritic cells (DCs), and cause tissue injuries to release danger-associated molecular patterns (DAMPs) such as adenosine triphosphate (ATP) and uric acid. Contaminating microbial pathogen-associated molecular patterns (PAMPs) associated or not with lipid-binding allergens trigger numerous pathogen recognition receptors (PRRs) which can produce also DAMPs whereas HDM glycan activation of DCs is mediated through C-type lectin receptors (CLR) ligation. These signaling pathways result in the upregulation of innate cytokines/chemokines such as IL-1β, IL-6, thymocyte stromal lymphpoetin (TSLP), IL-25, IL-33, GM-CSF, or CCL20 to recruit and activate inflammatory cells and to induce Th2 differentiation. TSLP mediates OX40L and IL-4 expression in DCs and basophils, respectively, to initiate a Th2-polarized response. IL-25 and IL-33 are strong activators of innate lymphocyte cells (ILC2s) which secrete theTh2 cytokine IL-13 to induce IgE secretion by B cells [40]. Modified from: Alain Jacquet, Innate immune responses in house dust mite allergy. IRSN Allergy 2013; 2013: 735031. DOI: 10.1155/2013/735031. The authors used Fig. 2 under the Creative Commons Attribution License