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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE214310 | GEO | 2023/11/30

REPOSITORIES: GEO

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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: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 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: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]

| PRJNA884831 | ENA

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

Oct1 and OCA-B are selectively required for CD4 memory T cell function.

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 memory. Yet the transcription factors that regulate these processes are poorly defined. We find that the transcription factor Oct1 and its cofactor OCA-B are selectively required for the in vivo generation of CD4(+) memory T cells. More importantly, the memory cells that are formed do not respond properly to antigen reencounter. In vitro, both proteins are required to maintain a poised state at the Il2 target locus in resting but previously stimulated CD4(+) T cells. OCA-B is also required for the robust reexpression of multiple other genes including Ifng. ChIPseq identifies ∼50 differentially expressed direct Oct1 and OCA-B targets. We identify an underlying mechanism involving OCA-B recruitment of the histone lysine demethylase Jmjd1a to targets such as Il2, Ifng, and Zbtb32. The findings pinpoint Oct1 and OCA-B as central mediators of CD4(+) T cell memory.

| S-EPMC4647264 | biostudies-literature

Oct1 and OCA-B are Selectively Required for CD4 Memory T Cell Formation and Function

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-09-17 | E-GEOD-65925 | biostudies-arrayexpress

Targeting transcriptional coregulator OCA-B/Pou2af1 blocks activated autoreactive T cells in the pancreas and type 1 diabetes.

Project description:The transcriptional coregulator OCA-B promotes expression of T cell target genes in cases of repeated antigen exposure, a necessary feature of autoimmunity. We hypothesized that T cell-specific OCA-B deletion and pharmacologic OCA-B inhibition would protect mice from autoimmune diabetes. We developed an Ocab conditional allele and backcrossed it onto a diabetes-prone NOD/ShiLtJ strain background. T cell-specific OCA-B loss protected mice from spontaneous disease. Protection was associated with large reductions in islet CD8+ T cell receptor specificities associated with diabetes pathogenesis. CD4+ clones associated with diabetes were present but associated with anergic phenotypes. The protective effect of OCA-B loss was recapitulated using autoantigen-specific NY8.3 mice but diminished in monoclonal models specific to artificial or neoantigens. Rationally designed membrane-penetrating OCA-B peptide inhibitors normalized glucose levels and reduced T cell infiltration and proinflammatory cytokine expression in newly diabetic NOD mice. Together, the results indicate that OCA-B is a potent autoimmune regulator and a promising target for pharmacologic inhibition.

| S-EPMC7731945 | biostudies-literature

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