麻省理工学院Gloria B. Choi课题组近日取得一项新成果。经过不懈努力，他们揭示了炎症和抗炎细胞因子双向调节杏仁核回路调节焦虑。2025年4月7日出版的《细胞》发表了这项成果。

研究人员表明，细胞因子作为神经调节剂，通过参与基底外侧杏仁核（BLA）中的受体表达神经元来调节焦虑。白细胞介素- 17a （IL-17A）和IL-17C水平升高，是由抗IL-17受体A （IL-17RA）抗体诱导的，通过增加表达IL-17RA/ re的BLA神经元的兴奋性来促进焦虑行为。相反，抗炎的IL-10，通过受体作用于同一群BLA神经元，对神经元的兴奋性和行为产生相反的影响。这些发现表明，炎症和抗炎细胞因子通过参与同一BLA群体中各自的受体来双向调节焦虑。他们的结果强调了细胞因子信号通过直接调节特定的神经基质在塑造内部状态中的作用。

据介绍，自身免疫性或感染性疾病患者在炎症发作后可出现持续的情绪改变。外周免疫分子，如细胞因子，可以影响行为和内部状态，但它们对大脑中特定神经回路功能的影响尚不清楚。

附：英文原文

Title: Inflammatory and anti-inflammatory cytokines bidirectionally modulate amygdala circuits regulating anxiety

Author: Byeongjun Lee, Jeong-Tae Kwon, Yire Jeong, Hannah Caris, Dongsun Oh, Mengyang Feng, Irene Davila Mejia, Xiaoying Zhang, Tomoe Ishikawa, Brianna R. Watson, Jeffrey R. Moffitt, Kwanghun Chung, Jun R. Huh, Gloria B. Choi

Issue&Volume: 2025-04-07

Abstract: Patients with autoimmune or infectious diseases can develop persistent mood alterations after inflammatory episodes. Peripheral immune molecules, like cytokines, can influence behavioral and internal states, yet their impact on the function of specific neural circuits in the brain remains unclear. Here, we show that cytokines act as neuromodulators to regulate anxiety by engaging receptor-expressing neurons in the basolateral amygdala (BLA). Heightened interleukin-17A (IL-17A) and IL-17C levels, paradoxically induced from treatment with anti-IL-17 receptor A (IL-17RA) antibodies, promote anxiogenic behaviors by increasing the excitability of IL-17RA/RE-expressing BLA neurons. Conversely, the anti-inflammatory IL-10, acting on the same population of BLA neurons via its receptor, exerts opposite effects on neuronal excitability and behavior. These findings reveal that inflammatory and anti-inflammatory cytokines bidirectionally modulate anxiety by engaging their respective receptors in the same BLA population. Our results highlight the role of cytokine signaling in shaping internal states through direct modulation of specific neural substrates.

DOI: 10.1016/j.cell.2025.03.005

Source: https://www.cell.com/cell/abstract/S0092-8674(25)00278-8