文献类型：期刊文献

英文题名：The role of peripheral innate immune cells in Alzheimer's disease progression

作者：Cao, Yanchun[1];Tang, Ke[2];Ma, Pengcheng[2];Zhang, Run[1];Yang, Yani[1];Li, Tingting[3];Zhang, Ying[4];Peng, Xiaoming[2]

第一作者：Cao, Yanchun

通信作者：Peng, XM[1]

机构：[1]Gansu Univ Chinese Med, Sch Tradit Chinese & Western Med, Lanzhou, Gansu, Peoples R China;[2]Gansu Univ Chinese Med, Affiliated Hosp, Dept Neurol, Lanzhou, Gansu, Peoples R China;[3]No 2 Peoples Hosp Lanzhou, Dept Psychiat, Lanzhou, Gansu, Peoples R China;[4]Xiaogan City Social Welf & Med Rehabil Ctr, Dept Psychiat, Xiaogan, Hubei, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Affiliated Hosp, Dept Neurol, Lanzhou, Gansu, Peoples R China.|[10735b845793de6ae2b30]甘肃中医药大学第二附属医院;[10735]甘肃中医药大学;

年份：2025

卷号：16

外文期刊名：FRONTIERS IN IMMUNOLOGY

收录：;Scopus(收录号：2-s2.0-105012036394);WOS:【SCI-EXPANDED(收录号:WOS:001538645600001)】；

基金：The author(s) declare that financial support was received for the research and/or publication of this article. This work was supported by Project of Gansu Provincial Administration of Chinese Medicine (GZKG-2024-59), Natural Science Foundation of Gansu Province (24JRRA1039). Gansu Province science and technology plan project (22JR11RA127).

语种：英文

外文关键词：Alzheimer's disease; peripheral innate immunity; neuroinflammation; trained immunity; genetic polymorphisms; myeloid-derived suppressor cells (MDSCs)

摘要：Alzheimer's disease (AD) is a neurodegenerative disorder characterized by amyloid-beta (A beta) plaques, neurofibrillary tangles, and chronic neuroinflammation. While microglia and astrocytes dominate CNS immune responses, emerging evidence implicates peripheral innate immune cells (PIICs)-including neutrophils, monocytes, dendritic cells, NK cells, and myeloid-derived suppressor cells (MDSCs)-as critical modulators of AD pathogenesis. This review synthesizes recent advances linking PIIC-related genetic polymorphisms to AD susceptibility and progression. We highlight how PIICs traffic into the brain via chemokine signaling, where they exhibit stage-specific effects: early recruitment may limit A beta deposition via phagocytosis, whereas chronic infiltration exacerbates neuroinflammation and neuronal death. Paradoxically, some PIICs exert immunosuppressive effects that could be harnessed therapeutically. We further discuss preclinical strategies to modulate PIIC function, such as CCR2 inhibition, neutrophil depletion, and MDSC adoptive transfer. By bridging peripheral and central immunity, this review unveils PIICs as promising targets for next-generation AD therapies, advocating for precision immunomodulation tailored to disease stages.