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Gut-licensed IFNγ+ NK cells drive LAMP1+TRAIL+ anti-inflammatory astrocytes
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Gut-licensed IFNγ+ NK cells drive LAMP1+TRAIL+ anti-inflammatory astrocytes
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Journal Article
Gut-licensed IFNγ+ NK cells drive LAMP1+TRAIL+ anti-inflammatory astrocytes
2021
Overview
Astrocytes are glial cells that are abundant in the central nervous system (CNS) and that have important homeostatic and disease-promoting functions
1
. However, little is known about the homeostatic anti-inflammatory activities of astrocytes and their regulation. Here, using high-throughput flow cytometry screening, single-cell RNA sequencing and CRISPR–Cas9-based cell-specific in vivo genetic perturbations in mice, we identify a subset of astrocytes that expresses the lysosomal protein LAMP1
2
and the death receptor ligand TRAIL
3
. LAMP1
+
TRAIL
+
astrocytes limit inflammation in the CNS by inducing T cell apoptosis through TRAIL–DR5 signalling. In homeostatic conditions, the expression of TRAIL in astrocytes is driven by interferon-γ (IFNγ) produced by meningeal natural killer (NK) cells, in which IFNγ expression is modulated by the gut microbiome. TRAIL expression in astrocytes is repressed by molecules produced by T cells and microglia in the context of inflammation. Altogether, we show that LAMP1
+
TRAIL
+
astrocytes limit CNS inflammation by inducing T cell apoptosis, and that this astrocyte subset is maintained by meningeal IFNγ
+
NK cells that are licensed by the microbiome.
A subpopulation of astrocytes characterized by the expression of LAMP1 and TRAIL limits inflammation in the central nervous system through a mechanism involving the microbiota-modulated expression of IFNγ in meningeal natural killer cells.
Publisher
Nature Publishing Group UK
Subject
/ 45/41
/ 45/47
/ 45/91
/ 64
/ 64/60
/ 96
/ 96/31
/ 96/35
/ 96/47
/ Animals
/ Central Nervous System - immunology
/ Encephalomyelitis, Autoimmune, Experimental - immunology
/ Encephalomyelitis, Autoimmune, Experimental - prevention & control
/ Female
/ Gastrointestinal Microbiome - immunology
/ Humanities and Social Sciences
/ Humans
/ Inflammation - prevention & control
/ Interferon-gamma - immunology
/ Killer Cells, Natural - immunology
/ Lysosomal Membrane Proteins - metabolism
/ Mice
/ Science
