Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CSF CD4+ T cells in MS

ABSTRACT: CSF CD4+ T cells in MS

PROVIDER: PRJNA721683 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14230100_1.fastq.gz	Fastqsanger.gz
	SRR14230100_2.fastq.gz	Fastqsanger.gz
	SRR14230101_1.fastq.gz	Fastqsanger.gz
	SRR14230101_2.fastq.gz	Fastqsanger.gz
	SRR14230102_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

scRNAseq of blood and CSF CD4+ T cells from MS patients and controls

Project description:To study the regulation of candidate genes from our study in human cells, we analyzed CD4+ T cells from blood and CSF of MA patients and age and sex matched idiopathic intracranial hypertension controls We analyzed 40845 cells in control blood, 807 cells in control CSF, 29749 cells in MS blood and 15768 cells in MS CSF

2023-08-01 | GSE232343 | GEO

scRNAseq of blood and CSF CD4+ T cells from MS patients and controls

Project description:scRNAseq of blood and CSF CD4+ T cells from MS patients and controls

| PRJNA971644 | ENA

Pro-inflammatory c-Met+ CD4 T cells in multiple sclerosis

Project description:Objective Hepatocyte growth factor (HGF) binds exclusively the c-Met surface receptor, and the HGF/c-Met axis regulates T-cell function in autoimmune diseases. We analyzed c-Met expression on human CD4 T cells in the blood and cerebrospinal fluid (CSF) from patients with multiple sclerosis (MS) versus non-inflammatory neurological disease (NIND), to better understand the role of CD4 T cells in MS. Methods We recruited 34 untreated MS patients (aged 28–43 years) and 10 NIND (aged 34–51 years) who underwent paired blood and CSF sampling at the time of diagnosis work-up. Phenotypic and functional CD4 T cells characterization was determined by flow cytometry and bulk RNA sequencing. Adhesion and transmigration capacities were studied to further characterize the function of c-Met+ CD4 T cells. Results c-Met+ memory CD4 T cells were detected at higher levels in both blood (median of 1.98%) and CSF (5.88%) in MS compared to NIND (0.37% and 0.68% respectively) (p<0.0001). Ex vivo c-Met+ CD4 T cells exhibited higher levels of GM-CSF, IL-17, IFN-γ and double positive IL-17+IFN-γ+ expression, compared with c-Met- CD4 T cells. c-Met+ CD4 T cells expressed increased levels of integrins – Itgα4β1 (VLA-4) and ItgαLβ2 (LFA-1) – compared with c-Met- CD4 T cells. Anti-Itgα4 (natalizumab) and anti-ItgαLβ2 (odulimomab) inhibited CD4 T cell transmigration with predominant inhibition of CD4 T cells expressing c-Met. Interpretation These results emphasize c-Met as an immune marker of highly pro-inflammatory and migratory CD4 T lymphocytes in both the periphery and central nervous system of MS patients.

2025-08-19 | GSE305678 | GEO

Single cell immune profiling reveals a developmentally distinct CD4+ GM-CSF+ T cell lineage that induces GI tract GVHD

Project description:Gastrointestinal (GI) tract involvement is a major determinant for subsequent morbidity and mortality arising during graft versus host disease (GVHD). CD4+ T cells that produce GM-CSF have emerged as central mediators of inflammation in this tissue site as GM-CSF serves as a critical cytokine link between the adaptive and innate arms of the immune system. However, cellular heterogeneity within the CD4+ GM-CSF+ T cell population due to the concurrent production of other inflammatory cytokines has raised questions as to whether these cells have a common ontology or if there exists a unique CD4+ GM-CSF+ subset that differs from other defined T helper (TH) subtypes. Using single cell RNA sequencing analysis, we identified two CD4+ GM-CSF+ T cell populations that arose during GVHD and were distinguishable by the presence or absence of IFN-γ co-expression. CD4+ GM-CSF+ IFN-γ- T cells which emerged preferentially in the colon had a distinct transcriptional profile, employed unique gene regulatory networks, and possessed a non-overlapping TCR repertoire when compared to CD4+ GM-CSF+ IFN-γ+ T cells as well as all other transcriptionally defined CD4+ T cell populations in the colon. Functionally, this CD4+ GM-CSF+ T cell population contributed to pathological damage in the GI tract which was critically dependent upon signaling through the IL-7 receptor but was independent of type 1 interferon signaling. Thus, these studies help to unravel heterogeneity within CD4+ GM-CSF+ T cells that arise during GVHD and define a developmentally distinct colitogenic TH GM-CSF+ subset that mediates immunopathology.

2022-01-14 | GSE193475 | GEO

Transcriptional profiling of brain CD4+ and CD8+ TRM cells reveals dominant presence in white and grey matter in Multiple Sclerosis (MS)

Project description:The human brain is populated by perivascular CD8+ and CD4+ T cells with a tissue-resident memory T (TRM)-cell phenotype. In multiple sclerosis (MS), these cells associate with white matter (WM) and, to a lesser extent, grey matter (GM) lesions. We here investigated the transcriptional and functional profile of brain-resident T cells. Of n=11 subsequent post-mortem brain donors, we isolated CD8+ and CD4+ effector memory and effector memory re-expressing CD45RA T cells from blood and CD8+ and CD4+ CD69+ T cells from corpus callosum WM and cortical GM. Additionally, brain CD69+ T cells were sorted from subcortical WM, corpus callosum WM, and medulla WM/GM of n=3–5 brain donors as well as from paired normal-appearing WM and GM and from WM and GM lesions of n=6 MS brain donors. In all donors, WM and GM T cells were overwhelmingly CD69+CD103+/-. Bulk RNA sequencing of CD8+ and CD4+ CD69+ T cells revealed TRM-cell signatures, as marked by differential expression of, among others, SELL (CD62L), ITGA1 (CD49a), and S1PR1. Notably, gene expression hardly differed between lesional and normal-appearing WM CD8+ and CD4+ CD69+ T cells in MS brains. Genes up-regulated in brain TRM cells were MS4A1 (CD20) and SPP1 (osteopontin, OPN). OPN is also abundantly expressed by microglia and has been shown to inhibit T-cell activity. In line with the increased presence of OPN in active MS lesions, we noticed a reduced production of the inflammatory cytokines IL-2, TNF, and IFNγ by MS lesion-derived CD8+ and CD4+ T cells ex vivo. This study discloses essential characteristics of human brain CD8+ and CD4+ TRM cells in non-MS and MS post-mortem WM and GM, reports OPN as a generic product of brain-resident immune cells, and shows a tight control of the activation state of TRM cells in MS lesions.

2022-12-05 | GSE216028 | GEO

CITE-seq of CD4+ T and myeloid cells in MS Twin cohort.

Project description:CITE-seq of CD4+ T and myeloid cells in MS Twin cohort.

| PRJNA795192 | ENA

mRNA-seq of the following human primary CD4 T cell subsets: GM-CSF producing, GM-CSF negative, bulk, memory and naive CD4 T cells.

Project description:mRNA-seq of the following human primary CD4 T cell subsets: GM-CSF producing, GM-CSF negative, bulk, memory and naive CD4 T cells.

| PRJNA490153 | ENA

ATAC-seq of the following human primary CD4 T cell subsets: GM-CSF producing, GM-CSF negative, bulk, memory and naive CD4 T cells.

Project description:ATAC-seq of the following human primary CD4 T cell subsets: GM-CSF producing, GM-CSF negative, bulk, memory and naive CD4 T cells.

| PRJNA490154 | ENA

Differential analysis of GM-CSF-induced inflammatory monocyte-derived cells (MCs) isolated from various organs

Project description:Elevated frequencies of GM-CSF-producing helper T (TH) cells are consistently found in multiple sclerosis (MS) patients and GM-CSF expression is a non-redundant feature of pathogenic TH cells in preclinical models of MS. GM-CSF activates an inflammatory signature in monocytes, and their progeny are the most abundant cellular infiltrate in acute MS lesions. To model deregulated GM-CSF levels, we generated a transgenic mouse line allowing the induction of GM-CSF expression in mature, peripheral TH cells. This antigen-independent GM-CSF release induced severe neurological deficits with almost 100% penetrance, accompanied by the infiltration of inflammatory monocyte-derived myeloid cells into the brain stem and spinal cord. Other organs did not show obvious signs for clinical pathology, despite also being infiltrated by inflammatory myeloid cells. We aim to unravel differences between organs, their responses and also the potential of tissue destruction by infiltrating cells by sequencing inflammatory myeloid cells isolate from the individual organs.

2017-02-21 | E-MTAB-5412 | biostudies-arrayexpress

CSF CD4+ T cells in MS

Project description:Single-cell transcriptome profiling of disease-related lymphocytes in patients with multiple sclerosis

2021-04-14 | GSE172003 | GEO