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OCA-B/Pou2af1 promotes autoimmune demyelination through control of stem-like CD4+ T cells [Bulk RNAseq]

ABSTRACT: OCA-B/Pou2af1 promotes autoimmune demyelination through control of stem-like CD4+ T cells [Bulk RNAseq]

PROVIDER: PRJNA1019708 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26142450_1.fastq.gz	Fastqsanger.gz
	SRR26142450_2.fastq.gz	Fastqsanger.gz
	SRR26142451_1.fastq.gz	Fastqsanger.gz
	SRR26142451_2.fastq.gz	Fastqsanger.gz
	SRR26142452_1.fastq.gz	Fastqsanger.gz

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OCA-B/Pou2af1 promotes autoimmune demyelination through control of stem-like CD4+ T cells [Bulk RNAseq]

Project description:The identification of druggable therapeutic targets that preferentially promote autoimmunity remains a key goal in the field. Recent work shows that populations of memory/stem-like T cells drive autoimmunity, but the factors that generate and sustain these populations are incompletely understood. The lymphocyte-restricted transcriptional cofactor OCA-B/Pou2af1 is a regulator of CD4+ T cell memory. Here we show that T cell-intrinsic loss of OCA-B protects mice from experimental autoimmune encephalomyelitis (EAE) in both chronic and relapsing-remitting mouse models while preserving acute responses to infection with a neurotropic coronavirus. In adoptive transfer EAE driven by antigen re-encounter, T cell-specific OCA-B loss largely eliminates Th1- and Th17-mediated CNS infiltration, proinflammatory cytokine production and disease. Using an OCA-B-mCherry reporter mouse, we show that OCA-B expressing CD4+ T cells within the CNS of mice with EAE preferentially display a memory-like phenotype. Transferring these OCA-Bhi memory-like CD4+ T cells preferentially confers disease, identifying OCA-B as a marker of encephalitogenic autoreactive CD4+ T cells. Notably, in a relapsing-remitting EAE model, OCA-B T cell-deficient mice show specific protection at relapse, highlighting the potential to target OCA-B in MS patients to limit disease progression. During remission, OCA-B promotes the expression of Tcf7, Slamf6, and Sell in proliferating T cell populations. At relapse, OCA-B loss results in the accumulation of an immunomodulatory CD4+ T cell population expressing Ccr9 and Bach2. These results highlight OCA-B as a driver of pathogenic stem-like T cells responsible for relapse and promising MS therapeutic target.

2024-04-09 | GSE243726 | GEO

OCA-B/Pou2af1 promotes autoimmune demyelination through control of stem-like CD4+ T cells

Project description:OCA-B/Pou2af1 promotes autoimmune demyelination through control of stem-like CD4+ T cells

| PRJNA1019704 | ENA

OCA-B/Pou2af1 promotes autoimmune demyelination through control of stem-like CD4+ T cells [Remission scRNAseq]

2024-04-09 | GSE243725 | GEO

OCA-B/Pou2af1 promotes autoimmune demyelination through control of stem-like CD4+ T cells [Relapse scRNAseq]

2024-04-09 | GSE243724 | GEO

OCA-B/Pou2af1 promotes autoimmune demyelination through control of stem-like CD4+ T cells [Relapse scRNAseq]

Project description:OCA-B/Pou2af1 promotes autoimmune demyelination through control of stem-like CD4+ T cells [Relapse scRNAseq]

| PRJNA1019707 | ENA

OCA-B/Pou2af1 promotes autoimmune demyelination through control of stem-like CD4+ T cells [Remission scRNAseq]

Project description:OCA-B/Pou2af1 promotes autoimmune demyelination through control of stem-like CD4+ T cells [Remission scRNAseq]

| PRJNA1019709 | ENA

Targeting OCA-B/Pou2af1 blocks type-1 diabetes and reduces infiltration of activated, islet-reactive T cells

Project description:The transcriptional coregulator OCA-B is induced in stimulated naïve CD4+ T cells, where docks with transcription factor Oct1 to regulate genes such as Il2 and Ifng. OCA-B regulates its targets in cases of repeated antigen exposure, a necessary feature of autoimmunity. Polymorphisms in binding sites for Oct1, and by extension OCA-B, as associated with multiple forms of autoimmunity including autoimmune (type-1) diabetes. We hypothesized that T cell-specific OCA-B deletion would protect mice from type-1 diabetes, and that pharmacologic OCA-B inhibition would provide similar protection. We developed an Ocab (Pou2af1) conditional allele and backcrossed it onto a diabetes-prone NOD/ShiLtJ strain background. T cell-specific OCA-B loss protected mice from spontaneous T1D. To clarify the mechanism, we profiled leukocytes from prediabetic islets by single-cell RNA sequencing and T cell receptor clonotype analysis.

2020-09-29 | GSE145228 | GEO

ChIP-seq for OCT2 and OCA-B in human primary naïve and germinal center B cells and germinal center B cell-derived cell lines following POU2AF1 knock down

Project description:ChIP-seq for OCT2 (POU2F2) and OCA-B (POU2AF1) in primary human tonsilar naïve and germinal center B cells, as well as germinal center B cell-derived cell lines following POU2AF1 knock down.

2021-09-11 | GSE183743 | GEO

OCA-B/Pou2af1 promotes autoimmune demyelination through control of stem-like CD4+ T cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-04-09 | GSE243727 | GEO

Effect of Pou2af1 on activated T cell transcriptome

Project description:Pou2af1 encodes for OCA-B, a coactivator of OCT-1/2. Although primarily studied in B cells, Pou2af1 mRNA expression is induced in activated T cells and T cells from B6.129S-Pou2af1-/- mice, bearing a mixed genetic background, show impaired T cell functions, such as cytokine production and Tfh differentiation. To revisit the impact of Pou2af1 in T cells, we generated Pou2af1fl/fl mice with specific genetic disruption of Pou2af1 in hematopoietic cells, Vav-Cre, or T cells, CD4-Cre, on the B6 background. Surprisingly, T cell cytokine production was not impaired in these models, and Tfh differentiation was influenced by T cell extrinsic deletion of Pou2af1. To determine the role of Pou2af1 induction in T cells, we performed RNA-Seq on activated T cells from CD4-Cre-.Pou2af1fl/fl and CD4-Cre+.Pou2af1fl/fl mice. Apart from Pou2af1 mRNA expression, the transcriptomic profiles were remarkably comparable. Overall, this study provides strong evidence that Pou2af1 does not act as transcriptional coactivator in T cells.

2022-03-24 | GSE171544 | GEO

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