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Neuroinflammation creates an immune regulatory niche at the meningeal lymphatic vasculature near the cribriform plate

ABSTRACT: Neuroinflammation creates an immune regulatory niche at the meningeal lymphatic vasculature near the cribriform plate

PROVIDER: PRJNA733769 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14689790_1.fastq.gz	Fastqsanger.gz
	SRR14689790_2.fastq.gz	Fastqsanger.gz
	SRR14689791_1.fastq.gz	Fastqsanger.gz
	SRR14689791_2.fastq.gz	Fastqsanger.gz
	SRR14689792_1.fastq.gz	Fastqsanger.gz

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Neuroinflammation creates an immune regulatory niche at the meningeal lymphatic vasculature near the cribriform plate

Project description:We report the use of single cell RNA sequencing of meningeal lymphatic endothelial cells near the cribriform plate in both naïve mice, and during experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis. By sorting for meningeal lymphatics near the cribriform plate, we identified that these lymphatic endothelial cells acquire an altered phenotype during neuroinflammation, where they become enriched in genes involved in leukocyte crosstalk including adhesion molecules, antigen processing and presentation, and tolerance, thus becoming a unique site of immune regulation.

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Neuroinflammation creates an immune regulatory niche at the meningeal lymphatic vasculature near the cribriform plate.

Project description:Meningeal lymphatics near the cribriform plate undergo lymphangiogenesis during neuroinflammation to drain excess fluid. Here, we hypothesized that lymphangiogenic vessels may acquire an altered phenotype to regulate immunity. Using single-cell RNA sequencing of meningeal lymphatics near the cribriform plate from healthy and experimental autoimmune encephalomyelitis in the C57BL/6 model, we report that neuroinflammation induces the upregulation of genes involved in antigen presentation such as major histocompatibility complex class II, adhesion molecules including vascular cell adhesion protein 1 and immunoregulatory molecules such as programmed cell death 1 ligand 1, where many of these changes are mediated by interferon-γ. The inflamed lymphatics retain CD11c+ cells and CD4 T cells where they capture and present antigen, creating an immunoregulatory niche that represents an underappreciated interface in the regulation of neuroinflammation. We also found discontinuity of the arachnoid membrane near the cribriform plate, which provides unrestricted access to the cerebrospinal fluid. These findings highlight a previously unknown function of local meningeal lymphatics in regulating immunity that has only previously been characterized in draining lymph nodes.

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