美国新泽西州立大学 Mark C. Siracusa研究组发现，嗜碱性粒细胞初免固有淋巴样细胞2亚类参与神经肽介导的抑制作用。这一研究成果于2020年8月17日在线发表在《自然-免疫学》上。

研究人员发现在没有嗜碱性粒细胞的情况下，蠕虫诱导的第2组先天淋巴样细胞（ILC2）反应过分激活，导致炎症增加和肺功能减弱。

此外，研究表明来自嗜碱性粒细胞减少小鼠的ILC2s减少了神经肽神经介素B（NMB）受体的表达。至关重要的是，NMB刺激抑制了对照组而非嗜碱性粒细胞减少小鼠的ILC2反应，并且嗜碱性粒细胞足以直接增强ILC2s上NMB受体的表达。

这些研究表明，嗜碱性粒细胞初免ILC2对维持组织完整性所必需的神经元衍生信号作出反应。此外，这些数据揭示了嗜碱性粒细胞发挥功能的机制，并确定NMB是2型炎症的有效抑制剂。

研究人员表示，Ⅱ型细胞因子反应促进寄生虫引起的免疫反应并启动组织修复。但是，如果限制不当，它们也会导致自身免疫病。尽管嗜碱性粒细胞被认为是2型炎症的共同特征，但仍然未知嗜碱性粒细胞在调节这些反应中的功能。

附：英文原文

Title: Basophils prime group 2 innate lymphoid cells for neuropeptide-mediated inhibition

Author: Juan M. Inclan-Rico, John J. Ponessa, Nuriban Valero-Pacheco, Christina M. Hernandez, Chandler B. Sy, Alexander D. Lemenze, Aimee M. Beaulieu, Mark C. Siracusa

Issue&Volume: 2020-08-17

Abstract: Type 2 cytokine responses promote parasitic immunity and initiate tissue repair; however, they can also result in immunopathologies when not properly restricted. Although basophilia is recognized as a common feature of type 2 inflammation, the roles basophils play in regulating these responses are unknown. Here, we demonstrate that helminth-induced group 2 innate lymphoid cell (ILC2) responses are exaggerated in the absence of basophils, resulting in increased inflammation and diminished lung function. Additionally, we show that ILC2s from basophil-depleted mice express reduced amounts of the receptor for the neuropeptide neuromedin B (NMB). Critically, NMB stimulation inhibited ILC2 responses from control but not basophil-depleted mice, and basophils were sufficient to directly enhance NMB receptor expression on ILC2s. These studies suggest that basophils prime ILC2s to respond to neuron-derived signals necessary to maintain tissue integrity. Further, these data provide mechanistic insight into the functions of basophils and identify NMB as a potent inhibitor of type 2 inflammation. Siracusa and colleagues reveal a regulatory role for basophils in the context of anti-helminth immunity and identify the neuropeptide neuromedin B as a potent inhibitor of type 2 inflammation.

DOI: 10.1038/s41590-020-0753-y

Source: https://www.nature.com/articles/s41590-020-0753-y