Group 2 innate lymphoid cells promote inhibitory synapse development and social behavior

IF 44.7 1区综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES Science Pub Date : 2024-11-01 DOI:10.1126/science.adi1025

Jerika J. Barron, Nicholas M. Mroz, Sunrae E. Taloma, Madelene W. Dahlgren, Jorge F. Ortiz-Carpena, Matthew G. Keefe, Caroline C. Escoubas, Leah C. Dorman, Ilia D. Vainchtein, Pailin Chiaranunt, Maya E. Kotas, Tomasz J. Nowakowski, Kevin J. Bender, Ari B. Molofsky, Anna V. Molofsky

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Abstract

The innate immune system shapes brain development and is implicated in neurodevelopmental diseases. It is critical to define the relevant immune cells and signals and their impact on brain circuits. In this work, we found that group 2 innate lymphoid cells (ILC2s) and their cytokine interleukin-13 (IL-13) signaled directly to inhibitory interneurons to increase inhibitory synapse density in the developing mouse brain. ILC2s expanded and produced IL-13 in the developing brain meninges. Loss of ILC2s or IL-13 signaling to interneurons decreased inhibitory, but not excitatory, cortical synapses. Conversely, ILC2s and IL-13 were sufficient to increase inhibitory synapses. Loss of this signaling pathway led to selective impairments in social interaction. These data define a type 2 neuroimmune circuit in early life that shapes inhibitory synapse development and behavior.

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第 2 组先天性淋巴细胞促进抑制性突触的发育和社交行为

先天性免疫系统影响大脑发育，并与神经发育疾病有关。确定相关的免疫细胞和信号及其对大脑回路的影响至关重要。在这项研究中，我们发现第2群先天性淋巴细胞（ILC2s）及其细胞因子白细胞介素-13（IL-13）直接向抑制性中间神经元发出信号，以增加发育中小鼠大脑的抑制性突触密度。ILC2s在发育中的脑膜中扩大并产生IL-13。失去ILC2s或IL-13对中间神经元的信号传导会减少大脑皮层的抑制性突触，但不会减少兴奋性突触。相反，ILC2s和IL-13足以增加抑制性突触。这种信号通路的缺失会导致社交互动的选择性障碍。这些数据定义了生命早期塑造抑制性突触发育和行为的2型神经免疫回路。

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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.