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. Author manuscript; available in PMC: 2017 Feb 1.
Published in final edited form as: Clin Exp Allergy. 2016 Feb;46(2):317–328. doi: 10.1111/cea.12612

Figure 6. Schematic of proposed pathway of innate allergic signaling mechanism in airway epithelial cells.

Figure 6

HDM and IL-17A activate p38 MAPK signaling in airway epithelial cells (AEC) to induce TNFα converting enzyme (TACE) or another member of the a disintegrin and metalloproteinases (ADAM) family to cleave EGFR ligands such as amphiregulin (AREG), on adjacent cells or on its own cell surface, that activate EGFR signaling, which drives the production of GM-CSF. GM-CSF contributes to allergic airway disease via the activation and priming of macrophages (Mϕ) to produce innate immune mediators and possibly through direct effects on the airway. Antigen presenting cells (APC) can process and present HDM antigens to activated T cells (Th1, Th2, Th17) that then release adaptive immune mediators and cytokines that contribute to the pathogenesis of allergic airway disease.