Vasoactive intestinal peptide confers anticipatory mucosal immunity by regulating ILC3 activity
Seillet, C.; Luong, K.; Tellier, J.; Jacquelot, N.; Shen, R. D.; Hickey, P.; Wimmer, V. C.; Whitehead, L.; Rogers, K.; Smyth, G.; Garnham, A.; Ritchie, M. E.; Belz, G.
Show abstract
ILC3-mediated IL-22 cytokine production is critical for the maintenance of immune homeostasis in the gastrointestinal tract. Here, we show that group 3 ILC (ILC3) constitutive function is not constant across the day but instead oscilliates between active and resting phases. Coordinate responsiveness of ILC3 in the intestine depended on food-induced expression of the neuronal hormone vasoactive intestinal peptide (VIP). Intestinal ILC3 expressed high levels of the G protein-coupled receptor, VIPR2, and activation via enteric neuronal VIP markedly enhanced IL-22 production and conferred gut protection. Conversely, deficiency of VIPR2 signalling led to impaired production of IL-22 by ILC3 and increased susceptibility to inflammatory gut disease. As such, intrinsic cellular rhythms synergise with the cyclic patterns of food intake to drive IL-22 thereby syncronizing intestinal epithelial protection via the ILC3 VIP-VIPR2 pathway.
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