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Fig. 2 | Inflammation and Regeneration

Fig. 2

From: The etiopathogenesis of atopic dermatitis: barrier disruption, immunological derangement, and pruritus

Fig. 2

Interplay among the barrier dysfunction, innate lymphoid cell (ILC)2, basophils, eosinophils, and mast cells. Barrier disruption leads to the production and release of epithelial-derived cytokines, namely, thymic stromal lymphopoietin (TSLP), IL-25, and IL-33. Upon ligation with the corresponding receptors on ILC2, TSLP receptor (TSLPR), IL-25 receptor (IL-25R, also known as IL17RB), and IL-33 receptor (IL-33R or ST2), ILC2 is activated to release Th2 cytokines, e.g., IL-5 and IL-13. In addition, IL-4 from basophils which are found in proximity to ILC2 in AD skin lesions can directly activate ILC2. PGD2, presumably from mast cell degranulation, also contributes to the recruitment of ILC2 into the skin as well as the induction of ILC2 Th2 cytokine production. In contrast, cell adhesion molecules, E-cadherin, on keratinocytes, are known to have an inhibitory effect on ILC2. Nevertheless, loss of E-cadherin is observed in FLG-deficient individuals. Therefore, skin inflammation is enhanced as there is an increase in stimulatory but a decrease in inhibitory stimuli

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