Fig. 3: Regulation of Helminth infection by enterochromaffin cells (ECCs), neurons, and neuronal mediators.
From: “Every cell is an immune cell; contributions of non-hematopoietic cells to anti-helminth immunity”
a Most work in the GI tract has examined multiple cellular sources of neurotransmitters serotonin (5-HT) and acetylcholine (Ach), including ILC2s, tuft cells, and ECCs. IL-33-evokes 5-HT release in ILC2 and ECCs. Serotonergic neurons (purple) activate cholinergic neurons (orange), which regulates the ISC. Ach can act on and be released by ILC2s, which also receive NMU signals from peptidergic neurons (red). Both inputs evoke the release of IL-13 from ILC2s. It is possible that some helminths may secrete AChEs to deplete Ach gradients in tissues. b Non-peptidergic neurons of the Mrgpr class (E, F) are reduced in density around encysted Sm eggs, but their role is unclear. c In the airway, ILC2s are positively regulated by NMU, while NMB and CGRP tend to inhibit their proliferation and type 2 cytokine secretion (although CGRP does not inhibit IL-5 secretion). Basophils induce the upregulation of the NMBR on ILC2s. The exact cellular source of CGRP and NMB are not clear. d Very little is known regarding multicellular crosstalk during helminth skin penetration, or if this is modulated by helminth E/S products.
