Immune Signaling in Neurodegeneration

被引：249
作者：
Hammond, Timothy R. [1 ,2 ,3 ]
Marsh, Samuel E. [1 ,2 ,3 ]
Stevens, Beth [1 ,2 ,3 ,4 ]
机构：
[1] Boston Childrens Hosp, FM Kirby Neurobiol Ctr, Boston, MA 02115 USA
[2] Harvard Med Sch, Boston, MA 02115 USA
[3] Broad Inst MIT & Harvard, Cambridge, MA 02142 USA
[4] Boston Childrens Hosp, Howard Hughes Med Inst, Boston, MA 02115 USA
来源：
IMMUNITY | 2019年 / 50卷 / 04期
基金：
美国国家卫生研究院;
关键词：
GENOME-WIDE ASSOCIATION; CENTRAL-NERVOUS-SYSTEM; MYELOID CELLS 2; FRONTOTEMPORAL LOBAR DEGENERATION; TRANSGENIC MOUSE MODEL; FLUID SOLUBLE TREM2; GROWTH-FACTOR-BETA; ANTI-A-BETA; ALZHEIMERS-DISEASE; AMYLOID-BETA;
D O I：
10.1016/j.immuni.2019.03.016
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
Neurodegenerative diseases of the central nervous system progressively rob patients of their memory, motor function, and ability to perform daily tasks. Advances in genetics and animal models are beginning to unearth an unexpected role of the immune system in disease onset and pathogenesis; however, the role of cytokines, growth factors, and other immune signaling pathways in disease pathogenesis is still being examined. Here we review recent genetic risk and genome-wide association studies and emerging mechanisms for three key immune pathways implicated in disease, the growth factor TGF-beta, the complement cascade, and the extracellular receptor TREM2. These immune signaling pathways are important under both healthy and neurodegenerative conditions, and recent work has highlighted new functional aspects of their signaling. Finally, we assess future directions for immune-related research in neurodegeneration and potential avenues for immune-related therapies.
引用
收藏
页码：955 / 974
页数：20
相关论文
共 281 条
[1]   iPSC-Derived Human Microglia-like Cells to Study Neurological Diseases [J].
Abud, Edsel M. ;
Ramirez, Ricardo N. ;
Martinez, Eric S. ;
Healy, Luke M. ;
Nguyen, Cecilia H. H. ;
Newman, Sean A. ;
Yeromin, Andriy V. ;
Scarfone, Vanessa M. ;
Marsh, Samuel E. ;
Fimbres, Cristhian ;
Caraway, Chad A. ;
Fote, Gianna M. ;
Madany, Abdullah M. ;
Agrawal, Anshu ;
Kayed, Rakez ;
Gylys, Karen H. ;
Cahalan, Michael D. ;
Cummings, Brian J. ;
Antel, Jack P. ;
Mortazavi, Ali ;
Carson, Monica J. ;
Poon, Wayne W. ;
Blurton-Jones, Mathew .
NEURON, 2017, 94 (02) :278-+
[2]   Localization and cell association of C1q in Alzheimer's disease brain [J].
Afagh, A ;
Cummings, BJ ;
Cribbs, DH ;
Cotman, CW ;
Tenner, AJ .
EXPERIMENTAL NEUROLOGY, 1996, 138 (01) :22-32
[3]  
Alzheimer A, 1911, EIGENARTIGE KRANKHEI
[4]  
Alzheimer A., 1907, ALLGEMEINE Z PSYCHIA, V64
[5]   Apolipoprotein E Is a Ligand for Triggering Receptor Expressed on Myeloid Cells 2 (TREM2) [J].
Atagi, Yuka ;
Liu, Chia-Chen ;
Painter, Meghan M. ;
Chen, Xiao-Fen ;
Verbeeck, Christophe ;
Zheng, Honghua ;
Li, Xia ;
Rademakers, Rosa ;
Kang, Silvia S. ;
Xu, Huaxi ;
Younkin, Steven ;
Das, Pritam ;
Fryer, John D. ;
Bu, Guojun .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2015, 290 (43) :26043-26050
[6]  
Bacskai BJ, 2002, J NEUROSCI, V22, P7873
[7]   The Triggering Receptor Expressed on Myeloid Cells 2 Binds Apolipoprotein E [J].
Bailey, Charles C. ;
DeVaux, Lindsey B. ;
Farzan, Michael .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2015, 290 (43) :26033-26042
[8]   The key role of T cells in Parkinson's disease pathogenesis and therapy [J].
Baird, Jill K. ;
Bourdette, Dennis ;
Meshul, Charles K. ;
Quinn, Joseph F. .
PARKINSONISM & RELATED DISORDERS, 2019, 60 :25-31
[9]   Frontotemporal dementia [J].
Bang, Jee ;
Spina, Salvatore ;
Miller, Bruce L. .
LANCET, 2015, 386 (10004) :1672-1682
[10]   Peripherally administered antibodies against amyloid β-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease [J].
Bard, F ;
Cannon, C ;
Barbour, R ;
Burke, RL ;
Games, D ;
Grajeda, H ;
Guido, T ;
Hu, K ;
Huang, JP ;
Johnson-Wood, K ;
Khan, K ;
Kholodenko, D ;
Lee, M ;
Lieberburg, I ;
Motter, R ;
Nguyen, M ;
Soriano, F ;
Vasquez, N ;
Weiss, K ;
Welch, B ;
Seubert, P ;
Schenk, D ;
Yednock, T .
NATURE MEDICINE, 2000, 6 (08) :916-919
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