Fig. 1: Induction of type II inflammation by various HDM-derived allergens. | Nature Immunology

Fig. 1: Induction of type II inflammation by various HDM-derived allergens.

From: A soluble allergen sensor sounds the alarm

Fig. 1

Allergen triggering of pattern recognition receptors (PRRs) induces activation of epithelial cells. Der p 1 is a cysteine protease that, together with various serine proteases (Der p 3, Der p 6 and Der p 9) that activate the protease-activated receptor 2 (PAR2), has the capacity to break down epithelial tight junctions (TJ). Der p 2 activates Toll-like receptor (TLR)2/4, leading to production of the indicated innate cytokines by epithelial cells. Smole and colleagues have identified a new pathway, dependent on the capacity of the fatty acid binding protein (FABP) allergen Der p 13 to induce dissociation of hexamers of the soluble PRR serum amyloid A (SAA), which results in epithelial IL-33 production via formyl peptide receptor-2 (FPR2) signaling. These epithelial proinflammatory signals induce the activation of group 2 innate lymphoid cells (ILC2s) and dendritic cells, which migrate to draining lymph nodes to present allergens to T cells, resulting in the differentiation of T helper 2 (TH2) cells that migrate to the lung. In the ensuing allergic airway inflammation, cardinal features of allergic asthma are attributed to cytokines that are produced by ILC2s and TH2 cells: IL-4 promotes class switching of allergen-specific B cells to IgE, IL-5 recruits eosinophils and IL-13 provokes goblet cell hyperplasia, mucus hyperproduction and smooth muscle hyperreactivity and impairs epithelial integrity. GM-CSF, granulocyte-macrophage colony-stimulating factor; TSLP, thymic stromal lymphopoietin.

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