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Comment
. 2018 Mar 14:9:230.
doi: 10.3389/fphar.2018.00230. eCollection 2018.

Commentary: Neuronal regulation of type 2 innate lymphoid cells via neuromedin U

Geraldine M Jowett  1   2 , Joana F Neves  2
Affiliations
Comment

Commentary: Neuronal regulation of type 2 innate lymphoid cells via neuromedin U

Geraldine M Jowett et al. Front Pharmacol. .
No abstract available

Keywords: IBD; innate lymphoid cells; mucosal epithelia; neuroimmunology; neuromedin U.

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Figures

Figure 1
Figure 1
Novel neuro-immune interactions in the mammalian gut. Cholinergic neural cells, type 2 innate lymphoid cells (ILC), and the intestinal epithelium orchestrate an innate response to N. brasiliensis worm infection (Left). Glial cells sense alarmins in the form of the helminth N. brasiliensis excretory/secretory products (NES) and the cytokine IL-33, that is secreted by damaged epithelium. This process is mediated by Myd88, and triggers the production and secretion of Neuromedin U (NMU). NMU induces smooth muscle contractions around the epithelium, which is hypothesized to help physically expulse the helminth infection, but is also recognized by the NMURI receptor specifically expressed on ILC2. NMU induces Ki67 mediated proliferation and activation of ILC2, which secrete type-2 cytokines [IL-5, IL-9, Il-13, amphiregulin (AREG)] to promote clearance of helminthic infection. A similar Myd88-dependent neuronal activation of ILC3 occurs when commensal microbiota induce neuronal activation of Ref-expressing ILC3 (Right), triggering the characteristic release of cytokine IL-22 to promote epithelial regeneration. Both receptors could be attractive therapeutic targets to modulate intestinal inflammation in IBD.
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