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Meningeal lymphoid structures are activated under acute and chronic spinal cord pathologies

ABSTRACT: Meningeal lymphoid structures are activated under acute and chronic spinal cord pathologies

PROVIDER: PRJNA672297 | ENA |

REPOSITORIES: ENA

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Meningeal lymphoid structures are activated under acute and chronic spinal cord pathologies

Project description:Tertiary lymphoid structures (TLS) are organized aggregates of B and T cells formed ectopically during different life periods in response to inflammation, infection, or cancer. Here, we describe formation of structures reminiscence of TLS in the spinal cord meninges under several central nervous system (CNS) pathologies. Following acute spinal cord injury, B and T lymphocytes locally aggregate within the meninges to form TLS, which continue to accumulate during the late phase of repair, with a negative impact on subsequent pathological conditions, such as experimental autoimmune encephalomyelitis. Using a chronic model of spinal cord pathology, the mSOD1 mouse model of amyotrophic lateral sclerosis, we further showed by single cell RNA-sequencing that a meningeal lymphocyte niche forms, with a unique organization and activation state, including accumulation of pre-B cells in the spinal cord meninges. Such a response was not found in the CNS-draining cervical lymph nodes. The present findings suggest that a unique immune response develops in the meninges during various neurological pathologies in the CNS, a reflection of its immune privileged nature.

2020-12-10 | GSE160193 | GEO

Meningeal lymphoid structures are activated under acute and chronic spinal cord pathologies.

Project description: Not available

| S-EPMC7723261 | biostudies-literature

Single cell analysis of meningeal ectopic lymphoid tissue and secondary lymphoid tissues in a spontaneous EAE model

Project description:Objective: To investigate how similar meningeal ectopic lymhpoid tissue (mELT) is to secondary lymphoid tissues and find unique features of mELT that could allow therapeutic targetting of mELT specifically. Methods: We utilized a spontaneous chronic experimental autoimmune encephalomyelitis (EAE) model of mice with mutant T and B cell receptors specific for myelin oligodendrocyte glycoprotein (MOG), which develop meningeal inflammatory infiltrates resembling those described in Multiple Sclerosis (MS). We identified differences in cell composition and gene expression between mELT and secondary lymphoid tissues (lumbar and inguinal lymph nodes and the spleen) using single cell sequencing.

2023-11-01 | GSE182774 | GEO

Meningeal natural killer cells and innate lymphoid cells 1 tune anxiety and memory via interferon-γ and acetylcholine

Project description:The mechanisms of communication between the brain and the neighboring meningeal immune cells are still unclear. Here we characterized the resident group 1 innate lymphoid cells in the meninges of adult mice, and identified ILC1/NK cell-derived interferon- and acetylcholine as mediators involved in the modulation of brain circuitries underlying anxiety-like behavior and memory. This discloses a new meningeal-to-brain communication mechanism that modulates brain functions under physiological conditions.

2023-05-05 | GSE212089 | GEO

Single cell analysis of meningeal ectopic lymphoid tissue and lumbar lymph nodes in a spontaneous EAE model

2023-11-01 | GSE181526 | GEO

Infiltrating B cells and tertiary lymphoid structures in the TME

Project description:Single-cell profiling of infiltrating B cells and tertiary lymphoid structures in the TME of gastric adenocarcinomas

2021-11-22 | GSE188895 | GEO

Gut-Resident IL10+CX3CR1hi Macrophages Induce Tertiary Lymphoid Structures and IgA Response in Situ

Project description:Gut resident IL10+CX3CR1hi macrophages drive development of mucosal tertiary lymphoid structures that serve as ectopic site of the IgA response to enteric infection.

2020-04-17 | GSE121471 | GEO

Effect of anti-CD20 treatment on the composition and gene expression of meningeal ectopic lymphoid tissue and CSFin a spontaneous EAE model, using single cell gene expression .

Project description:Objective: To investigate how anti-CD20 B cell-depleting monoclonal antibodies (ɑCD20 mAb) alter the composition and gene expression of immune cells in meningeal ectopic lymphoid tissue (mELT) and the CSF in a murine model of Multiple Sclerosis (MS). Methods: We utilized a spontaneous chronic experimental autoimmune encephalomyelitis (EAE) model of mice with mutant T and B cell receptors specific for myelin oligodendrocyte glycoprotein (MOG), which develop meningeal inflammatory infiltrates resembling those described in Multiple Sclerosis (MS). We studied the changes in cell composition and gene expression after anti-CD20 treatment in mELT and CSF.

2023-11-01 | GSE181506 | GEO

Infiltrating B cells and tertiary lymphoid structures in the TME

Project description:Infiltrating B cells and tertiary lymphoid structures in the TME

| PRJNA780577 | ENA

Loss of Vascular Endothelial Notch Signaling Induces Tertiary Lymphoid Structures in the Kidney

Project description:Tertiary lymphoid structures (TLS are lymph node-like immune cell clusters that emerge during chronic inflammation in non-lymphoid organs like the kidney, but their origin remains not well understood. Here we show, using conditional deletion strategies of the canonical Notch signaling mediator Rbpj, that loss of endothelial Notch signaling in adult mice induces the spontaneous formation of bona fide TLS in the kidney, liver and lung, based on molecular, cellular and structural criteria. These TLS form in a stereotypical manner around parenchymal arteries, while secondary lymphoid structures remained largely unchanged. This effect is mediated by endothelium of blood vessels, but not lymphatics, since a lymphatic endothelial-specific targeting strategy did not result in TLS formation, and involves loss of arterial specification and concomitant acquisition of a high endothelial cell phenotype, as shown by transcriptional analysis of kidney endothelial cells. This indicates a so far unrecognized role for vascular endothelial cells and Notch signaling in TLS initiation.

2022-02-24 | GSE193544 | GEO

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