TREM2 regulates innate immunity in Alzheimer's disease

被引：53

作者：

Li, Jiang-Tao ^{[1
]}

Zhang, Ying ^{[1
]}

机构：

[1] Beijing Jiaotong Univ, Coll Life Sci & Bioengn, 3 Shangyuan Residence, Beijing 100044, Peoples R China

来源：

JOURNAL OF NEUROINFLAMMATION | 2018年 / 15卷

基金：

中国国家自然科学基金; 北京市自然科学基金;

关键词：

Alzheimer's disease (AD); Triggering receptor expressed on myeloid cells 2 (TREM2); Innate immunity; Inflammation; MYELOID CELLS 2; FLUID SOLUBLE TREM2; TOLL-LIKE RECEPTORS; CEREBROSPINAL-FLUID; RISK-FACTOR; INFLAMMATORY RESPONSES; UP-REGULATION; A-BETA; MICROGLIA; VARIANTS;

D O I：

10.1186/s12974-018-1148-y

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Recent research has shown that the triggering receptor expressed on myeloid cells 2 (TREM2) in microglia is closely related to the pathogenesis of Alzheimer's disease (AD). The mechanism of this relationship, however, remains unclear. TREM2 is part of the TREM family of receptors, which are expressed primarily in myeloid cells, including monocytes, dendritic cells, and microglia. The TREM family members are cell surface glycoproteins with an immunoglobulin-like extracellular domain, a transmembrane region and a short cytoplasmic tail region. The present article reviews the following: (1) the structure, function, and variant site analysis of the Trem2 gene; (2) the metabolism of TREM2 in peripheral blood and cerebrospinal fluid; and (3) the possible underlying mechanism by which TREM2 regulates innate immunity and participates in AD.

引用

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