Gene expression during CCK-induced damaged pancreatic acinar cells with or without the addition of OCA
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1029978 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26440687_1.fastq.gz | Fastqsanger.gz | |||
| SRR26440687_2.fastq.gz | Fastqsanger.gz | |||
| SRR26440688_1.fastq.gz | Fastqsanger.gz | |||
| SRR26440688_2.fastq.gz | Fastqsanger.gz | |||
| SRR26440689_1.fastq.gz | Fastqsanger.gz |
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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.
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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.
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