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OCA-B/Pou2af1 is sufficient to promote CD4+ T cell memory and prospectively identifies memory precursors [single cell RNA-Seq]

ABSTRACT: OCA-B/Pou2af1 is sufficient to promote CD4+ T cell memory and prospectively identifies memory precursors [single cell RNA-Seq]

PROVIDER: PRJNA884831 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21729507.fastq.gz	Fastqsanger.gz
	SRR21729508.fastq.gz	Fastqsanger.gz
	SRR21729509.fastq.gz	Fastqsanger.gz
	SRR21729510.fastq.gz	Fastqsanger.gz

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OCA-B/Pou2af1 is sufficient to promote CD4 memory and prospectively identifies memory precursors

Project description:OCA-B/Pou2af1 is sufficient to promote CD4 memory and prospectively identifies memory precursors

| PRJNA884727 | ENA

OCA-B/Pou2af1 is sufficient to promote CD4+ T cell memory and prospectively identifies memory precursors [bulk RNA-Seq]

Project description:Sun et al. use T cell conditional knockout and ectopic expression to show that OCA-B is required for, and sufficient to promote, CD4+ memory T cell formation in vivo, and can be used to prospectively identify effector T cells with enhanced memory potential.

2023-11-30 | GSE214307 | GEO

OCA-B/Pou2af1 is sufficient to promote CD4+ T cell memory and prospectively identifies memory precursors [single cell RNA-Seq]

2023-11-30 | GSE214308 | GEO

OCA-B/Pou2af1 is sufficient to promote CD4+ T cell memory and prospectively identifies memory precursors [bulk RNA-Seq]

Project description:OCA-B/Pou2af1 is sufficient to promote CD4+ T cell memory and prospectively identifies memory precursors [bulk RNA-Seq]

| PRJNA884832 | ENA

OCA-B/Pou2af1 is sufficient to promote CD4<sup>+</sup> T cell memory and prospectively identifies memory precursors.

Project description:The molecular mechanisms leading to the establishment of immunological memory are inadequately understood, limiting the development of effective vaccines and durable antitumor immune therapies. Here, we show that ectopic OCA-B expression is sufficient to improve antiviral memory recall responses, while having minimal effects on primary effector responses. At peak viral response, short-lived effector T cell populations are expanded but show increased Gadd45b and Socs2 expression, while memory precursor effector cells show increased expression of Bcl2, Il7r, and Tcf7 on a per-cell basis. Using an OCA-B mCherry reporter mouse line, we observe high OCA-B expression in CD4+ central memory T cells. We show that early in viral infection, endogenously elevated OCA-B expression prospectively identifies memory precursor cells with increased survival capability and memory recall potential. Cumulatively, the results demonstrate that OCA-B is both necessary and sufficient to promote CD4 T cell memory in vivo and can be used to prospectively identify memory precursor cells.

| S-EPMC10907311 | biostudies-literature

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 [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 is sufficient to promote CD4 memory and prospectively identifies memory precursors

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

2023-11-30 | GSE214310 | 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

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