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. 2019 Dec 4;19(2):809–816. doi: 10.3892/etm.2019.8283

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Copyright: © Ren et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 2. — The signalling pathway through which NMU activates ILC2s. NMU activates ILC2s via NMUR1, which is a GPCR. The activated G protein receptor activates PLC, which catalyses the conversion of the phospholipid inositol to DAG and IP3. Subsequently, IP₃ elicits Ca²⁺ release from intracellular stores. The increased Ca²⁺ influx triggers ERK phosphorylation and activates the Ca²⁺ calcineurin/NFAT cascade, inducing the increased expression of the type 2 cytokine genes IL-5, IL-13 and Areg. ILC2s, type 2 innate lymphoid cells; GPCR, G protein-coupled receptor; ERK, extracellular signal-regulated kinase; NFAT, nuclear factor of activated T cells; NMU, neuromedin U; NMUR, neuromedin U receptor; p-, phosphorylated; PLC, phospholipase C; DAG, diacylglycerol; IP₃, inositol 1,4,5-trisphosphate.