Alzheimer’s disease alters the transcriptomic profile of natural killer cells at single-cell resolution

Alzheimer’s disease (AD) is the most common dementia without an effective cure at least partially due to incomplete understanding of the disease. Inflammation has emerged as a central player in the onset and progression of AD. As innate lymphoid cells, natural killer (NK) cells orchestrate the initi...

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Veröffentlicht in:Frontiers in immunology Jg. 13; S. 1004885
Hauptverfasser: Qi, Caiyun, Liu, Fang, Zhang, Wenjun, Han, Yali, Zhang, Nan, Liu, Qiang, Li, Handong
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Switzerland Frontiers Media S.A 02.11.2022
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Abstract Alzheimer’s disease (AD) is the most common dementia without an effective cure at least partially due to incomplete understanding of the disease. Inflammation has emerged as a central player in the onset and progression of AD. As innate lymphoid cells, natural killer (NK) cells orchestrate the initiation and evolution of inflammatory responses. Yet, the transcriptomic features of NK cells in AD remain poorly understood. We assessed the diversity of NK cells using web-based single-cell RNA sequencing data of blood NK cells from patients with AD and control subjects and flow cytometry. We identified a contraction of NK cell compartment in AD, accompanied by a reduction of cytotoxicity. Unbiased clustering revealed four subsets of NK cells in AD, i.e., CD56 bright NK cells, CD56 dim effector NK cells, adaptive NK cells, and a unique NK cell subset that is expanded and characterized by upregulation of CX3CR1, TBX21, MYOM2, DUSP1, and ZFP36L2, and negatively correlated with cognitive function in AD patients. Pseudo-temporal analysis revealed that this unique NK cell subset was at a late stage of NK cell development and enriched with transcription factors TBX21, NFATC2, and SMAD3. Together, our study identified a distinct NK cell subset and its potential involvement in AD.
AbstractList Alzheimer's disease (AD) is the most common dementia without an effective cure at least partially due to incomplete understanding of the disease. Inflammation has emerged as a central player in the onset and progression of AD. As innate lymphoid cells, natural killer (NK) cells orchestrate the initiation and evolution of inflammatory responses. Yet, the transcriptomic features of NK cells in AD remain poorly understood. We assessed the diversity of NK cells using web-based single-cell RNA sequencing data of blood NK cells from patients with AD and control subjects and flow cytometry. We identified a contraction of NK cell compartment in AD, accompanied by a reduction of cytotoxicity. Unbiased clustering revealed four subsets of NK cells in AD, i.e., CD56 NK cells, CD56 effector NK cells, adaptive NK cells, and a unique NK cell subset that is expanded and characterized by upregulation of CX3CR1, TBX21, MYOM2, DUSP1, and ZFP36L2, and negatively correlated with cognitive function in AD patients. Pseudo-temporal analysis revealed that this unique NK cell subset was at a late stage of NK cell development and enriched with transcription factors TBX21, NFATC2, and SMAD3. Together, our study identified a distinct NK cell subset and its potential involvement in AD.
Alzheimer’s disease (AD) is the most common dementia without an effective cure at least partially due to incomplete understanding of the disease. Inflammation has emerged as a central player in the onset and progression of AD. As innate lymphoid cells, natural killer (NK) cells orchestrate the initiation and evolution of inflammatory responses. Yet, the transcriptomic features of NK cells in AD remain poorly understood. We assessed the diversity of NK cells using web-based single-cell RNA sequencing data of blood NK cells from patients with AD and control subjects and flow cytometry. We identified a contraction of NK cell compartment in AD, accompanied by a reduction of cytotoxicity. Unbiased clustering revealed four subsets of NK cells in AD, i.e., CD56bright NK cells, CD56dim effector NK cells, adaptive NK cells, and a unique NK cell subset that is expanded and characterized by upregulation of CX3CR1, TBX21, MYOM2, DUSP1, and ZFP36L2, and negatively correlated with cognitive function in AD patients. Pseudo-temporal analysis revealed that this unique NK cell subset was at a late stage of NK cell development and enriched with transcription factors TBX21, NFATC2, and SMAD3. Together, our study identified a distinct NK cell subset and its potential involvement in AD.
Alzheimer's disease (AD) is the most common dementia without an effective cure at least partially due to incomplete understanding of the disease. Inflammation has emerged as a central player in the onset and progression of AD. As innate lymphoid cells, natural killer (NK) cells orchestrate the initiation and evolution of inflammatory responses. Yet, the transcriptomic features of NK cells in AD remain poorly understood. We assessed the diversity of NK cells using web-based single-cell RNA sequencing data of blood NK cells from patients with AD and control subjects and flow cytometry. We identified a contraction of NK cell compartment in AD, accompanied by a reduction of cytotoxicity. Unbiased clustering revealed four subsets of NK cells in AD, i.e., CD56bright NK cells, CD56dim effector NK cells, adaptive NK cells, and a unique NK cell subset that is expanded and characterized by upregulation of CX3CR1, TBX21, MYOM2, DUSP1, and ZFP36L2, and negatively correlated with cognitive function in AD patients. Pseudo-temporal analysis revealed that this unique NK cell subset was at a late stage of NK cell development and enriched with transcription factors TBX21, NFATC2, and SMAD3. Together, our study identified a distinct NK cell subset and its potential involvement in AD.Alzheimer's disease (AD) is the most common dementia without an effective cure at least partially due to incomplete understanding of the disease. Inflammation has emerged as a central player in the onset and progression of AD. As innate lymphoid cells, natural killer (NK) cells orchestrate the initiation and evolution of inflammatory responses. Yet, the transcriptomic features of NK cells in AD remain poorly understood. We assessed the diversity of NK cells using web-based single-cell RNA sequencing data of blood NK cells from patients with AD and control subjects and flow cytometry. We identified a contraction of NK cell compartment in AD, accompanied by a reduction of cytotoxicity. Unbiased clustering revealed four subsets of NK cells in AD, i.e., CD56bright NK cells, CD56dim effector NK cells, adaptive NK cells, and a unique NK cell subset that is expanded and characterized by upregulation of CX3CR1, TBX21, MYOM2, DUSP1, and ZFP36L2, and negatively correlated with cognitive function in AD patients. Pseudo-temporal analysis revealed that this unique NK cell subset was at a late stage of NK cell development and enriched with transcription factors TBX21, NFATC2, and SMAD3. Together, our study identified a distinct NK cell subset and its potential involvement in AD.
Alzheimer’s disease (AD) is the most common dementia without an effective cure at least partially due to incomplete understanding of the disease. Inflammation has emerged as a central player in the onset and progression of AD. As innate lymphoid cells, natural killer (NK) cells orchestrate the initiation and evolution of inflammatory responses. Yet, the transcriptomic features of NK cells in AD remain poorly understood. We assessed the diversity of NK cells using web-based single-cell RNA sequencing data of blood NK cells from patients with AD and control subjects and flow cytometry. We identified a contraction of NK cell compartment in AD, accompanied by a reduction of cytotoxicity. Unbiased clustering revealed four subsets of NK cells in AD, i.e., CD56 bright NK cells, CD56 dim effector NK cells, adaptive NK cells, and a unique NK cell subset that is expanded and characterized by upregulation of CX3CR1, TBX21, MYOM2, DUSP1, and ZFP36L2, and negatively correlated with cognitive function in AD patients. Pseudo-temporal analysis revealed that this unique NK cell subset was at a late stage of NK cell development and enriched with transcription factors TBX21, NFATC2, and SMAD3. Together, our study identified a distinct NK cell subset and its potential involvement in AD.
Author Qi, Caiyun
Zhang, Nan
Li, Handong
Liu, Qiang
Zhang, Wenjun
Liu, Fang
Han, Yali
AuthorAffiliation Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital , Tianjin , China
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Cites_doi 10.1038/s43587-022-00198-9
10.1016/j.jneuroim.2005.02.011
10.3389/fimmu.2021.768966
10.1016/j.immuni.2018.09.009
10.2147/jir.s4397
10.1038/s41467-019-14118-w
10.1038/s41467-019-11947-7
10.1038/s41423-020-00574-8
10.1038/nn.4211
10.1038/s41590-018-0212-1
10.1002/ana.22339
10.1038/nm.3913
10.1101/cshperspect.a006346
10.1038/s41593-020-00745-w
10.1016/j.ebiom.2020.102686
10.1038/ni.3368
10.4049/jimmunol.2000037
10.3389/fimmu.2021.645666
10.4049/jimmunol.1300090
10.1523/JNEUROSCI.0829-08.2008
10.1523/JNEUROSCI.0616-08.2008
10.1016/j.cell.2021.04.048
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Keywords single cell sequencing
Alzheimer’s disease
innate immunity
natural killer cell
cytotoxicity
Language English
License Copyright © 2022 Qi, Liu, Zhang, Han, Zhang, Liu and Li.
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Edited by: Lan Wu, Vanderbilt University Medical Center, United States
This article was submitted to NK and Innate Lymphoid Cell Biology, a section of the journal Frontiers in Immunology
Reviewed by: Anil Shanker, Meharry Medical College, United States; Seokmann Hong, Sejong University, South Korea; Lindsay Celada, Baylor College of Medicine, United States
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References Wyss-Coray (B3) 2012; 2
Hao (B10) 2021; 184
Luo (B11) 2022; 2
Hao (B8) 2011; 69
Yang (B15) 2019; 10
Cai (B16) 2020; 53
Zenaro (B6) 2015; 21
Ponzetta (B19) 2013; 191
Lu (B21) 2021; 12
Liu (B22) 2016; 19
Maier (B2) 2008; 28
Xu (B7) 2005; 163
Crinier (B14) 2021; 18
McAlpine (B1) 2008; 1
Crinier (B13) 2018; 49
Hickman (B4) 2008; 28
Schafflick (B12) 2020; 11
Xu (B9) 2021; 12
Zhang (B20) 2020; 205
Song (B5) 2018; 19
Bjorklund (B17) 2016; 17
Jin (B23) 2021; 24
Ponzetta (B18) 2013; 191
References_xml – volume: 2
  year: 2022
  ident: B11
  article-title: Multidimensional single-cell analysis of human peripheral blood reveals characteristic features of the immune system landscape in aging and frailty
  publication-title: Nat Aging
  doi: 10.1038/s43587-022-00198-9
– volume: 163
  start-page: 24
  year: 2005
  ident: B7
  article-title: Mechanism of natural killer (Nk) cell regulatory role in experimental autoimmune encephalomyelitis
  publication-title: J Neuroimmunol
  doi: 10.1016/j.jneuroim.2005.02.011
– volume: 12
  year: 2021
  ident: B21
  article-title: Expression of immune related genes and possible regulatory mechanisms in alzheimer's disease
  publication-title: Front Immunol
  doi: 10.3389/fimmu.2021.768966
– volume: 49
  start-page: 971
  year: 2018
  ident: B13
  article-title: High-dimensional single-cell analysis identifies organ-specific signatures and conserved nk cell subsets in humans and mice
  publication-title: Immunity
  doi: 10.1016/j.immuni.2018.09.009
– volume: 1
  start-page: 29
  year: 2008
  ident: B1
  article-title: Neuroinflammation and tumor necrosis factor signaling in the pathophysiology of alzheimer's disease
  publication-title: J Inflamm Res
  doi: 10.2147/jir.s4397
– volume: 11
  start-page: 247
  year: 2020
  ident: B12
  article-title: Integrated single cell analysis of blood and cerebrospinal fluid leukocytes in multiple sclerosis
  publication-title: Nat Commun
  doi: 10.1038/s41467-019-14118-w
– volume: 10
  start-page: 3931
  year: 2019
  ident: B15
  article-title: Heterogeneity of human bone marrow and blood natural killer cells defined by single-cell transcriptome
  publication-title: Nat Commun
  doi: 10.1038/s41467-019-11947-7
– volume: 18
  year: 2021
  ident: B14
  article-title: Single-cell profiling reveals the trajectories of natural killer cell differentiation in bone marrow and a stress signature induced by acute myeloid leukemia
  publication-title: Cell Mol Immunol
  doi: 10.1038/s41423-020-00574-8
– volume: 19
  year: 2016
  ident: B22
  article-title: Neural stem cells sustain natural killer cells that dictate recovery from brain inflammation
  publication-title: Nat Neurosci
  doi: 10.1038/nn.4211
– volume: 19
  year: 2018
  ident: B5
  article-title: The identity and function of microglia in neurodegeneration
  publication-title: Nat Immunol
  doi: 10.1038/s41590-018-0212-1
– volume: 69
  year: 2011
  ident: B8
  article-title: Interleukin-2/Interleukin-2 antibody therapy induces target organ natural killer cells that inhibit central nervous system inflammation
  publication-title: Ann Neurol
  doi: 10.1002/ana.22339
– volume: 21
  year: 2015
  ident: B6
  article-title: Neutrophils promote alzheimer's disease-like pathology and cognitive decline Via lfa-1 integrin
  publication-title: Nat Med
  doi: 10.1038/nm.3913
– volume: 2
  year: 2012
  ident: B3
  article-title: Inflammation in Alzheimer disease-a brief review of the basic science and clinical literature
  publication-title: Cold Spring Harb Perspect Med
  doi: 10.1101/cshperspect.a006346
– volume: 24
  start-page: 61
  year: 2021
  ident: B23
  article-title: Neuroblast senescence in the aged brain augments natural killer cell cytotoxicity leading to impaired neurogenesis and cognition
  publication-title: Nat Neurosci
  doi: 10.1038/s41593-020-00745-w
– volume: 53
  year: 2020
  ident: B16
  article-title: Single-cell transcriptomics of blood reveals a natural killer cell subset depletion in tuberculosis
  publication-title: EBioMedicine
  doi: 10.1016/j.ebiom.2020.102686
– volume: 17
  year: 2016
  ident: B17
  article-title: The heterogeneity of human Cd127(+) innate lymphoid cells revealed by single-cell rna sequencing
  publication-title: Nat Immunol
  doi: 10.1038/ni.3368
– volume: 205
  year: 2020
  ident: B20
  article-title: Depletion of nk cells improves cognitive function in the Alzheimer disease mouse model
  publication-title: J Immunol
  doi: 10.4049/jimmunol.2000037
– volume: 12
  year: 2021
  ident: B9
  article-title: Single-cell rna sequencing of peripheral blood reveals immune cell signatures in alzheimer's disease
  publication-title: Front Immunol
  doi: 10.3389/fimmu.2021.645666
– volume: 191
  year: 2013
  ident: B18
  article-title: Cx3cr1 regulates the maintenance of Klrg1+ nk cells into the bone marrow by promoting their entry into circulation
  publication-title: J Immunol
  doi: 10.4049/jimmunol.1300090
– volume: 28
  year: 2008
  ident: B2
  article-title: Complement C3 deficiency leads to accelerated amyloid beta plaque deposition and neurodegeneration and modulation of the Microglia/Macrophage phenotype in amyloid precursor protein transgenic mice
  publication-title: J Neurosci
  doi: 10.1523/JNEUROSCI.0829-08.2008
– volume: 28
  year: 2008
  ident: B4
  article-title: Microglial dysfunction and defective beta-amyloid clearance pathways in aging alzheimer's disease mice
  publication-title: J Neurosci
  doi: 10.1523/JNEUROSCI.0616-08.2008
– volume: 184
  start-page: 3573
  year: 2021
  ident: B10
  article-title: Integrated analysis of multimodal single-cell data
  publication-title: Cell
  doi: 10.1016/j.cell.2021.04.048
– volume: 191
  year: 2013
  ident: B19
  article-title: Cx3cr1 regulates the maintenance of Klrg1(+) nk cells into the bone marrow by promoting their entry into circulation
  publication-title: J Immunol
  doi: 10.4049/jimmunol.1300090
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Snippet Alzheimer’s disease (AD) is the most common dementia without an effective cure at least partially due to incomplete understanding of the disease. Inflammation...
Alzheimer's disease (AD) is the most common dementia without an effective cure at least partially due to incomplete understanding of the disease. Inflammation...
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StartPage 1004885
SubjectTerms Alzheimer Disease - genetics
Alzheimer’s disease
CD56 Antigen - analysis
CD56 Antigen - genetics
cytotoxicity
Humans
Immunity, Innate
Immunology
innate immunity
Killer Cells, Natural
natural killer cell
single cell sequencing
Transcriptome
Title Alzheimer’s disease alters the transcriptomic profile of natural killer cells at single-cell resolution
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https://pubmed.ncbi.nlm.nih.gov/PMC9666759
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