Neuronal-ILC2 interactions regulate pancreatic glucagon and glucose homeostasis

IF 44.7 1区综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES

Science Pub Date : 2025-01-16 DOI:10.1126/science.adi3624

Marko Šestan, Bruno Raposo, Miguel Rendas, David Brea, Roksana Pirzgalska, Ana Rasteiro, Maria Aliseychik, Inês Godinho, Hélder Ribeiro, Tania Carvalho, Stephan Wueest, Daniel Konrad, Henrique Veiga-Fernandes

引用次数: 0

Abstract

The immune system shapes body metabolism, while interactions between peripheral neurons and immune cells control tissue homeostasis and immunity. However, whether peripheral neuroimmune interactions orchestrate endocrine system functions remains unexplored. After fasting, mice lacking type 2 innate lymphoid cells (ILC2s) displayed disrupted glucose homeostasis, impaired pancreatic glucagon secretion, and inefficient hepatic gluconeogenesis. Additionally, intestinal ILC2s were found in the pancreas, which was dependent on their expression of the adrenergic beta 2 receptor. Targeted activation of catecholaminergic intestinal neurons promoted the accumulation of ILC2s in the pancreas. Our work provides evidence that immune cells can be regulated by neuronal signals in response to fasting, activating an inter-organ communication route that promotes pancreatic endocrine function and regulation of blood glucose levels.

查看原文本刊更多论文

神经元- ilc2相互作用调节胰高血糖素和葡萄糖稳态

免疫系统塑造机体代谢，而外周神经元和免疫细胞之间的相互作用控制着组织稳态和免疫。然而，周围神经免疫相互作用是否协调内分泌系统功能仍未研究。禁食后，缺乏2型先天淋巴样细胞（ILC2s）的小鼠表现出葡萄糖稳态被破坏，胰高血糖素分泌受损，肝脏糖异生效率低下。此外，在胰腺中发现了肠道ILC2s，这依赖于它们对肾上腺素能β 2受体的表达。靶向激活肠道儿茶酚胺能神经元可促进胰腺中ILC2s的积累。我们的工作提供了证据，证明免疫细胞可以受到神经元信号的调节，以响应禁食，激活器官间通讯途径，促进胰腺内分泌功能和调节血糖水平。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Science 综合性期刊-综合性期刊

CiteScore

61.10

自引率

0.90%

发文量

审稿时长

2.1 months

期刊介绍： Science is a leading outlet for scientific news, commentary, and cutting-edge research. Through its print and online incarnations, Science reaches an estimated worldwide readership of more than one million. Science’s authorship is global too, and its articles consistently rank among the world's most cited research. Science serves as a forum for discussion of important issues related to the advancement of science by publishing material on which a consensus has been reached as well as including the presentation of minority or conflicting points of view. Accordingly, all articles published in Science—including editorials, news and comment, and book reviews—are signed and reflect the individual views of the authors and not official points of view adopted by AAAS or the institutions with which the authors are affiliated. Science seeks to publish those papers that are most influential in their fields or across fields and that will significantly advance scientific understanding. Selected papers should present novel and broadly important data, syntheses, or concepts. They should merit recognition by the wider scientific community and general public provided by publication in Science, beyond that provided by specialty journals. Science welcomes submissions from all fields of science and from any source. The editors are committed to the prompt evaluation and publication of submitted papers while upholding high standards that support reproducibility of published research. Science is published weekly; selected papers are published online ahead of print.