神经肽血管活性肠肽（VIP）通过调节3型先天性淋巴样细胞（ILC3）活性赋予肠道粘膜免疫力，这一成果由澳大利亚墨尔本大学Gabrielle T. Belz、Cyril Seillet等研究人员合作完成。2019年12月23日，《自然—免疫学》在线发表了这一最新研究成果。

研究人员发现ILC3的功能并非整天都是恒定的，而是在活跃期和休息期之间振荡。肠道中ILC3的协调反应取决于食物诱导的神经肽VIP的表达。肠道ILC3具有高表达的G蛋白偶联受体血管活性肠肽受体2（VIPR2），而VIP激活显著增强了白介素22（IL-22）的产生和上皮的屏障功能。相反，VIPR2的信号转导不足会导致ILC3减少IL-22的产生，并增加对炎症诱发的肠道损伤敏感性。因此，固有的细胞节律与食物摄入的循环模式协同作用，以驱动IL-22的产生并通过ILC3中的VIP-VIPR2途径同步保护肠上皮。

研究人员表示，ILC3介导的细胞因子IL-22的产生对于维持胃肠道免疫稳态是至关重要的。

附：英文原文

Title: The neuropeptide VIP confers anticipatory mucosal immunity by regulating ILC3 activity

Author: Cyril Seillet, Kylie Luong, Julie Tellier, Nicolas Jacquelot, Rui Dong Shen, Peter Hickey, Verena C. Wimmer, Lachlan Whitehead, Kelly Rogers, Gordon K. Smyth, Alexandra L. Garnham, Matthew E. Ritchie, Gabrielle T. Belz

Issue&Volume: 2019-12-23

Abstract: Group 3 innate lymphoid cell (ILC3)-mediated production of the cytokine interleukin-22 (IL-22) is critical for the maintenance of immune homeostasis in the gastrointestinal tract. Here, we find that the function of ILC3s is not constant across the day, but instead oscillates between active phases and resting phases. Coordinate responsiveness of ILC3s in the intestine depended on the food-induced expression of the neuropeptide vasoactive intestinal peptide (VIP). Intestinal ILC3s had high expression of the G protein-coupled receptor vasoactive intestinal peptide receptor 2 (VIPR2), and activation by VIP markedly enhanced the production of IL-22 and the barrier function of the epithelium. Conversely, deficiency in signaling through VIPR2 led to impaired production of IL-22 by ILC3s and increased susceptibility to inflammation-induced gut injury. Thus, intrinsic cellular rhythms acted in synergy with the cyclic patterns of food intake to drive the production of IL-22 and synchronize protection of the intestinal epithelium through a VIP–VIPR2 pathway in ILC3s.

DOI: 10.1038/s41590-019-0567-y

Source: https://www.nature.com/articles/s41590-019-0567-y