美国麻省理工学院Gloria B. Choi团队揭示了IL-1R1阳性中缝背神经元驱动疾病中自我强加的社交退缩。相关论文发表在2025年11月25日出版的《细胞》杂志上。

通过行为筛选，该研究团队确定了细胞因子白细胞介素-1β (IL-1β)在疾病期间促进社交退缩中的独特作用。IL-1β直接调节中缝背核（DRN）中表达IL-1R1的神经元（IL-1R1DRN）的活性。这些神经元的激活足以引发社交退缩，而它们对IL-1R1的抑制或基因缺失则可以在全身性炎症期间挽救自我强加的社交隔离。他们的发现揭示了一种积极促进患病动物脱离社会的神经机制，强调了IL-1R1DRN神经元在驱动这些行为适应中的作用。

据介绍，患病动物表现出的行为变化超出了生理症状，如食欲不振和活动不足，还包括社交活动减少。虽然疾病期间的社会隔离已被认为具有避免疾病传播的进化益处，但这种反应背后的分子和神经机制尚不清楚。细胞因子-免疫衍生的信号分子-已经成为炎症期间影响大脑功能的神经调节剂。

附：英文原文

Title: IL-1R1-positive dorsal raphe neurons drive self-imposed social withdrawal in sickness

Author: Liu Yang, Matias L. Andina, Mario Witkowski, Hunter King, Ian Wickersham, Jun R. Huh, Gloria B. Choi

Issue&Volume: 2025-11-25

Abstract: Sick animals exhibit behavioral changes that extend beyond physiological symptoms, such as appetite loss and hypoactivity, and include a decline in social interactions. While social isolation during sickness has been recognized to have the evolutionary benefit of staving off disease spread, the molecular and neural mechanisms underlying this response remain unclear. Cytokines—immune-derived signaling molecules—have emerged as neuromodulators impacting brain function during inflammation. Through behavioral screening, we identify a unique role for the cytokine interleukin-1β (IL-1β) in promoting social withdrawal during sickness. IL-1β directly modulates the activity of IL-1R1-expressing neurons in the dorsal raphe nucleus (DRN) (IL-1R1DRN). Activation of these neurons is sufficient to elicit social withdrawal, while their inhibition or genetic deletion of IL-1R1 rescues self-imposed social isolation during systemic inflammation. Our findings reveal a neural mechanism that actively promotes social disengagement in sick animals, highlighting the role of IL-1R1DRN neurons in driving these behavioral adaptations.

DOI: 10.1016/j.cell.2025.10.040

Source: https://www.cell.com/cell/abstract/S0092-8674(25)01245-0