Figure 2 Key brain–immune–gut interactions

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Figure 2 Key brain–immune–gut interactions Figure 2 | Key brain–immune–gut interactions. There is complex crosstalk between the immune system, the brain and the gut. Noradrenergic neurons in the gut release noradrenaline (NA), which ligates the β2 adrenergic receptor (β2AR) on macrophages in the myenteric plexus (supporting differentiation towards the M2 phenotype) and T cells, which limits T helper (TH)1 differentiation (indirectly favouring TH2 and TH17 differentiation). Mast cells and eosinophils are found degranulating next to enteric neurons, providing a mechanism for sensory excitation (which can be perceived by the enteric nervous system (ENS) and central nervous system). Gut immune cells (e.g. γδ T cells) differentiating in the gut can traffic to the brain under some circumstances (e.g. after brain injury). Blood-borne cytokines generated in the gut can also signal in the brain. Enteric glial cells also produce glial-cell-derived neurotrophic factor family ligands (GFL), which stimulate IL-22 production by innate lymphoid cell (ILC)3 (acting on the specific receptor RET). IL-22 acts on an epithelial-restricted receptor (IL-22R) to stimulate epithelial proliferation, antimicrobial peptide production. IL-4 and IL-5 (potentially generated locally by TH2 T cells) support activation of mast cells and eosinophils, respectively. AMP, antimicrobial peptides. Powell, N. et al. (2017) The mucosal immune system: master regulator of bidirectional gut–brain communications Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2016.191