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. 2021 Sep 1;15(1):27–39. doi: 10.1038/s41385-021-00443-1

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© The Author(s) 2021, corrected publication 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — In brief, ISNs (which originate in the myenteric plexus but have multiple long processes allowing them to contact cells in the lamina propria) represent the sole source of NMU in the GI tract and can also secrete CGRPα and ACh. Of note, ISNs also express receptors for IL-4 and IL-13, and a subset of these neurons express the NMU receptor, Nmur2. Thus, ISNs have the potential to participate in bi-directional communication with ILC2s during homeostasis and following helminth infection. In the submucosal plexus cholinergic vasodilator/secretomotor neurons secrete ACh and potentially CGRPα and therefore may also interact with ILC2s, whilst non-cholinergic vasodilator/secretomotor neurons may interact with homeostatic ILC2s via their secretion of VIP. Extrinsic primary afferent neurons may also regulate ILC2 activities via CGRPα. Creative Commons Attribution 3.0 Unported (CC BY 3.0).