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Nat Neurosci. 2018 Apr;21(4):541-551. doi: 10.1038/s41593-018-0100-x. Epub 2018 Mar 5.

Single-cell mass cytometry reveals distinct populations of brain myeloid cells in mouse neuroinflammation and neurodegeneration models.

Author information

1
Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA. b.ajami@stanford.edu.
2
Baxter Laboratory in Stem Cell Biology, Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA, USA.
3
Institute of Neuropathology, Medical Faculty, University of Freiburg, Freiburg, Germany.
4
Institute of Anatomy, University of Leipzig, Leipzig, Germany.
5
Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
6
Department of Cellular and Molecular Medicine, University of California, San Diego, La Jolla, CA, USA.
7
BIOSS Centre for Biological Signalling Studies, University of Freiburg, Freiburg, Germany.
8
Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA. steinman@stanford.edu.

Abstract

Neuroinflammation and neurodegeneration may represent two poles of brain pathology. Brain myeloid cells, particularly microglia, play key roles in these conditions. We employed single-cell mass cytometry (CyTOF) to compare myeloid cell populations in the experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis, the R6/2 model of Huntington's disease (HD) and the mutant superoxide dismutase 1 (mSOD1) model of amyotrophic lateral sclerosis (ALS). We identified three myeloid cell populations exclusive to the CNS and present in each disease model. Blood-derived monocytes comprised five populations and migrated to the brain in EAE, but not in HD and ALS models. Single-cell analysis resolved differences in signaling and cytokine production within similar myeloid populations in EAE compared to HD and ALS models. Moreover, these analyses highlighted α5 integrin on myeloid cells as a potential therapeutic target for neuroinflammation. Together, these findings illustrate how neuropathology may differ between inflammatory and degenerative brain disease.

PMID:
29507414
DOI:
10.1038/s41593-018-0100-x
[Indexed for MEDLINE]

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