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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE214307 | GEO | 2023/11/30

REPOSITORIES: GEO

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OCA-B/Pou2af1 is sufficient to promote CD4+ T cell memory and prospectively identifies memory precursors [single cell 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 | GSE214308 | GEO

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

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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 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+ T cell memory and prospectively identifies memory precursors [single cell RNA-Seq]

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

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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

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

Oct1 and OCA-B are Selectively Required for CD4 Memory T Cell Formation and Function (ChIP-seq)

Project description:Epigenetic changes are crucial for the generation of immunological memory. Failure to generate or maintain these changes will result in poor memory responses. Similarly, augmenting or stabilizing the correct epigenetic states offers a potential method of enhancing immune memory. Yet the transcription factors that regulate these processes are poorly defined, as are the target genes they control and they chromatin-modifying complexes they recruit. Using model pathogens and three different mouse models, we find that the widely expressed transcription factor Oct1 and its cofactor OCA-B are selectively required for the in vivo generation of functional CD4 memory. In vitro, both proteins are required to maintain a poised state at the Il2 target locus in resting but previously stimulated CD4 T cells, and to generate robust Il2 expression upon restimulation. Gene expression profiling indicates that OCA-B is also required for the robust re-expression of multiple other targets including Ifng and Il17a. ChIPseq identify multiple differentially expressed direct targets. We identify an underlying mechanism involving OCA-B recruitment of the histone lysine demethylase Jmjd1a to targets such as Il2 and Ifng. The findings pinpoint Oct1 and OCA-B as unanticipated mediators of CD4 T cell memory. Examination of transcription factor occupancy in CD4 T cells upon rest and restimulation.

2015-09-17 | E-GEOD-65918 | biostudies-arrayexpress

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