载脂蛋白 E4 影响阿尔茨海默病中的中性粒细胞-小胶质细胞相互作用。

APOE4 affects neutrophil-microglia crosstalk in Alzheimer's disease.

机构信息

Department of Medicine, University of Verona, Strada le Grazie 8, 37134 Verona, Italy.

Department of Medicine, University of Verona, Strada le Grazie 8, 37134 Verona, Italy; The Center for Biomedical Computing (CBMC), University of Verona, 37134 Verona, Italy.

出版信息

Trends Immunol. 2024 Oct;45(10):726-728. doi: 10.1016/j.it.2024.09.002. Epub 2024 Sep 24.

DOI:10.1016/j.it.2024.09.002

PMID:39322476

Abstract

Circulating immune cells contribute to the pathogenesis of Alzheimer's disease (AD), but their role is poorly understood. Rosenzweig et al. recently identified a subset of interleukin (IL)-17 neutrophils that inhibit neuroprotective microglia in female APOE4 carriers. Blockade of IL-17 signaling or APOE4 deletion in neutrophils restored microglial responses and reduced murine amyloid pathology.

摘要

循环免疫细胞有助于阿尔茨海默病（AD）的发病机制，但它们的作用尚未被充分了解。Rosenzweig 等人最近发现了一种白细胞介素（IL）-17 中性粒细胞亚群，它可以抑制 APOE4 携带者的神经保护性小胶质细胞。中性粒细胞中 IL-17 信号的阻断或 APOE4 的缺失恢复了小胶质细胞的反应，减少了小鼠淀粉样蛋白病理。