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NF-κB transcription factors RelA and c-Rel selectively control CD4+ T-cell function in multiple sclerosis and cancer [bulk_mouse]

ABSTRACT: NF-κB transcription factors RelA and c-Rel selectively control CD4+ T-cell function in multiple sclerosis and cancer [bulk_mouse]

PROVIDER: PRJNA1000591 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25469902_1.fastq.gz	Fastqsanger.gz
	SRR25469902_2.fastq.gz	Fastqsanger.gz
	SRR25469903_1.fastq.gz	Fastqsanger.gz
	SRR25469903_2.fastq.gz	Fastqsanger.gz
	SRR25469904_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

NF-κB transcription factors RelA and c-Rel selectively control CD4+ T-cell function in multiple sclerosis and cancer [bulk_human]

Project description:The outcome of cancer and autoimmunity is dictated by the recruitment and effector functions of CD4+ conventional T cells (Tconv cells). The NF-kappaB (NF-κB) family of transcription factors is implicated in different aspects of Tconv cell biology, but the cell-autonomous roles of NF-κB subunits are elusive. Here, we explored the contributions of canonical RelA and c-Rel subunits to Tconv function in health and disease. We found that RelA, rather than c-Rel, shaped the transcriptome of mouse and human Tconv cells at steady-state and was required for Tconv polarization toward the TH17 lineage in vitro. RelA-deficient mice were fully protected against neuro-inflammation in a mouse model of multiple sclerosis (MS), because of defective transition to a pathogenic TH17 gene expression program. In contrast, Tconv-restricted ablation of c-Rel, but not RelA, impaired their function in the microenvironment of transplanted tumors, resulting in enhanced cancer burden. c-Rel in Tconv cells was required for the response to PD-1-blockade therapy, and a c-Rel-dependent gene signature was correlated with better response and prognosis in anti-PD-1-treated patients. Our data demonstrate a division of labor between different subunits of the NF-κB pathway, paving the way for subunit-targeted immunotherapies.

2024-03-28 | GSE239698 | GEO

NF-κB transcription factors RelA and c-Rel selectively control CD4+ T-cell function in multiple sclerosis and cancer [sc_rna]

2024-03-28 | GSE239703 | GEO

NF-κB transcription factors RelA and c-Rel selectively control CD4+ T-cell function in multiple sclerosis and cancer [bulk_mouse]

2024-03-28 | GSE239700 | GEO

NF-κB transcription factors RelA and c-Rel selectively control CD4+ T-cell function in multiple sclerosis and cancer

Project description:NF-κB transcription factors RelA and c-Rel selectively control CD4+ T-cell function in multiple sclerosis and cancer

| PRJNA1000587 | ENA

Transcriptional profiling of NF-kB's Rel and RelA proteins

Project description:Rel and RelA proteins were stably expressed in the chicken DT40 pre-B cell line and analyzed by transcription profiling to identify transformation-impacting genes regulated by NF-kB’s oncogenic v-Rel and c-Rel proteins. This analysis uncovered both common and differential gene expression profiles in cells expressing Rel vs. RelA proteins, and revealed that Rel protein expression can lead to gene-specific transcriptional repression, as seen for key B-cell receptor (BCR) components and signaling molecules like B-cell linker (BLNK), the B-cell adaptor for PI3K (BCAP) and Igλ. These were also downregulated in cells expressing a transformation-competent chimeric RelA/v-Rel protein, suggesting a correlation with the capacity of Rel proteins to transform lymphocytes. DNA binding, ChIP and transformation assays indicate that downregulation of BLNK and BCAP is an important contributing factor to the malignant transformation of lymphocytes by Rel and suggest that gene repression may be as important as transcriptional activation for the transforming activity of Rel proteins. Keywords: Comparative transcriptional profiling

2008-02-14 | GSE9544 | GEO

NF-κB transcription factors RelA and c-Rel selectively control CD4+ T-cell function in multiple sclerosis and cancer [bulk_human]

Project description:NF-κB transcription factors RelA and c-Rel selectively control CD4+ T-cell function in multiple sclerosis and cancer [bulk_human]

| PRJNA1000589 | ENA

NF-κB transcription factors RelA and c-Rel selectively control CD4+ T-cell function in multiple sclerosis and cancer [sc_rna]

Project description:NF-κB transcription factors RelA and c-Rel selectively control CD4+ T-cell function in multiple sclerosis and cancer [sc_rna]

| PRJNA1000594 | ENA

Positive and negative regulation of lymphomagenesis by the NF-kappaB subunit c-Rel

Project description:'The REL gene, encoding the NF-κB subunit c-Rel, is frequently amplified in B-cell lymphoma and functions as a tumour promoting transcription factor. Here we report the surprising result that c-rel -/- mice display significantly earlier lymphomagenesis in the c-Myc driven, Eμ-Myc model of B-cell lymphoma. c-Rel loss also led to earlier onset of disease in a separate TCL1-Tg driven lymphoma model. Tumour reimplantation experiments indicated that this is an effect intrinsic to the Eμ-Myc lymphoma cells but, counter-intuitively, c-rel -/- Eμ-Myc lymphoma cells were more sensitive to apoptotic stimuli. To learn more about why loss of c-Rel led to earlier onset of disease, microarray gene expression analysis was performed on B-cells from 4-week old, wild type and c-rel -/- Eμ-Myc mice. Extensive changes in gene expression were not seen at this age but among those transcripts significantly downregulated by the loss of c-Rel was the B-cell tumour suppressor BTB and CNC homology 2 (Bach2). Q-PCR and western blot analysis confirmed loss of Bach2 in c-Rel mutant Eμ-Myc tumours at both 4 weeks and the terminal stages of disease. Moreover Bach2 expression was also downregulated in c-rel -/- TCL1-Tg mice and RelA Thr505Ala mutant Eμ-Myc mice. Analysis of wild type Eμ-Myc mice demonstrated that the population expressing low levels of Bach2 exhibited the earlier onset of lymphoma seen in c-rel-/- mice. Confirming the relevance of these findings to human disease, analysis of ChIP-Seq data revealed that Bach2 is a c-Rel and NF-κB target gene in transformed human B-cells, while treatment of Burkitt''s lymphoma cells with inhibitors of the NF-κB/IKK pathway or deletion of c-Rel or RelA resulted in loss of Bach2 expression. This data reveals a surprising tumour suppressor role for c-Rel in lymphoma development explained by regulation of Bach2 expression, underlining the context dependent complexity of NF-κB signalling in cancer.'

2014-12-31 | E-MTAB-2774 | biostudies-arrayexpress

NF-κB subunits RelA and c-Rel selectively control CD4+ T cell function in multiple sclerosis and cancer.

Project description:The outcome of cancer and autoimmunity is often dictated by the effector functions of CD4+ conventional T cells (Tconv). Although activation of the NF-κB signaling pathway has long been implicated in Tconv biology, the cell-autonomous roles of the separate NF-κB transcription-factor subunits are unknown. Here, we dissected the contributions of the canonical NF-κB subunits RelA and c-Rel to Tconv function. RelA, rather than c-Rel, regulated Tconv activation and cytokine production at steady-state and was required for polarization toward the TH17 lineage in vitro. Accordingly, RelA-deficient mice were fully protected against neuroinflammation in a model of multiple sclerosis due to defective transition to a pathogenic TH17 gene-expression program. Conversely, Tconv-restricted ablation of c-Rel impaired their function in the microenvironment of transplanted tumors, resulting in enhanced cancer burden. Moreover, Tconv required c-Rel for the response to PD-1-blockade therapy. Our data reveal distinct roles for canonical NF-κB subunits in different disease contexts, paving the way for subunit-targeted immunotherapies.

| S-EPMC10986815 | biostudies-literature

Identification of c-Rel and RelA binding regions in stimulated EL4 cells

Project description:c-Rel and RelA are members of the NF-kappaB family of transcription factors. They both have important roles in T cell activation. To discover where in the genome c-Rel and RelA bind and hence which genes they may directly target, we used ChIP-chip with EL4 cells stimulated with phorbol ester (PMA) and Ionomycin. We have identified regions in EL4 cells (background strain: C57BL/6N) activated for 2h or 8h by PMA and Ionomycin, that bind the transcription factors c-Rel and RelA. Immunoprecipitated samples from EL4 cells stimulated with PMA and ionomycin for 2 h and 8 h with antibodies against RelA or c-Rel respectively were used for ChIP-on-chip experiments. In addition, samples from total input and mock immunoprecipitation were used as controls. Biological triplicates were used.

2013-12-29 | E-GEOD-42818 | biostudies-arrayexpress

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