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RELA tunes innate-like interferon I/III responses in human T cells

ABSTRACT: RELA tunes innate-like interferon I/III responses in human T cells

PROVIDER: PRJNA757358 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15595156_1.fastq.gz	Fastqsanger.gz
	SRR15595156_2.fastq.gz	Fastqsanger.gz
	SRR15595157_1.fastq.gz	Fastqsanger.gz
	SRR15595157_2.fastq.gz	Fastqsanger.gz
	SRR15595160_1.fastq.gz	Fastqsanger.gz

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RELA tunes innate-like interferon I/III responses in human T cells

Project description:In innate immune cells, intracellular sensors such as cGAS-STING stimulate type I/III interferon (IFN) expression, which promotes antiviral defense and immune activation. However, how IFN-I/III expression is controlled in adaptive cells is poorly understood. Here, we identify a transcriptional rheostat orchestrated by RELA that confers human T cells with innate-like abilities to produce IFN-I/III. Despite intact cGAS-STING signaling, IFN-I/III responses are stunted in CD4+ T cells compared with dendritic cells or macrophages. We find that lysine residues in RELA tune the IFN-I/III response at baseline and in response to STING stimulation in CD4+ T cells. This response requires positive feedback driven by cGAS and IRF7 expression. By combining RELA with IRF3 and DNA demethylation, IFN-I/III production in CD4+ T cells reaches levels observed in dendritic cells. IFN-I/III production provides self-protection of CD4+ T cells against HIV infection and enhances the elimination of tumor cells by CAR T cells. Therefore, innate-like functions can be tuned and leveraged in human T cells.

2023-02-16 | GSE182647 | GEO

RELA tunes innate-like interferon I/III responses in human T cells.

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Transcriptome profiling of murine overexpression of p65/RelA mutants III

Project description:Transcriptome profiling of murine overexpression of p65/RelA mutants III

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Identification of genes responsible for RelA-dependent proliferation arrest in HMEC conditionally expressing RelA

Project description:Immuno-histochemistry for RelA in breast tumors revealed a range of staining intensity and negative correlation between RelA levels and proliferation-index in estrogen receptor-positive tumors. Conditional expression of RelA arrested proliferation in primary mammary and fallopian tube epithelial cells. RelA dependent CDK4 downregulation was responsible for activating the G1/S checkpoint and cell cycle arrest. RelA target genes, including Interferon Response Factors (IRF), were up-regulated in the arrested cells. Among the IRFs, IRF1 expression correlates with RelA expression. Suppressing IRF1 restored CDK4 levels and rescued RelA-dependent proliferation arrest analogous to abrogating the G1/S checkpoint or restoring CDK4 levels. Apart from cyclins, regulation of CDK4 by the RelA-IRF1 transcriptional network controls proliferation of breast tumors and predicts sensitivity to a CDK4/6 inhibitor.

2015-09-26 | GSE65040 | GEO

Transcription factor TFII-I fine tunes innate properties of B lymphocytes

Project description:Transcription factor TFII-I fine tunes innate properties of B lymphocytes

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Transcriptional Responses of Human Intestinal Organoids to Interferon Types I, II, and III

Project description:RNAseq of intestinal epithelial cell (IEC) organoids derived from biopsy of ileum or colon from healthy subjects and treated with type I interferon (IFN beta), type II interferon (IFN gamma), or type III interferon (IFN lambda 2).

2021-12-21 | GSE190899 | GEO

NS7a of SADS-CoV promotes viral infection via inducing apoptosis to suppress Type III interferon production

Project description:SADS-CoV is a newly discovered swine coronavirus with potential cross-species transmission risk. Although SADS-CoV-induced host cell apoptosis and attenuated innate immunity has been established, the relation between apoptosis and innate immunity remain obscure. Here, we demonstrate that infection of SADS-CoV induced apoptosis in vivo and in vitro, and that viral protein NS7a is mainly responsible for SADS-CoV-induced apoptosis in host cells. Furthermore, we found that NS7a interacted with apoptosis inducing factor mitochondria associated 1 (AIFM1) to activate caspase-3 via caspase-6 in SADS-CoV-infected cells, and enhanced SADS-CoV replication. Importantly, NS7a suppressed Poly(I:C)-induced expression of Type III interferon (IFN-λ) via activation caspase-3 to cleave IRF3, and caspase-3 inhibitor protects piglets against SADS-CoV infection in vivo. These findings reveal how SADS-CoV-induced apoptosis to inhibit innate immunity and provide a valuable clue to the development of effective drugs for the clinical control of SADS-CoV infection.

2025-05-06 | PXD047032 | Pride

Differential response of polarized gut epithelial cells to type I and III interferon

Project description:Whereas most body cells respond to stimulation with type I (alpha and beta) interferon, type III (lambda) interferon was shown to specifically stimulate epithelial cells in the gastrointestinal and respiratory tract. Although both cytokines activate different receptor molecules (IFNAR versus IL-28R/IL-10R, respectively) the downstream signalling pathways and the ultimate response have been reported to be very similar. Here we examined the response of polarized gut intestinal epithelial cells to type I versus type III interferon in order to study potential differences in the transcriptional response.

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Transcriptome profiling of murine overexpression of p65/RelA mutants III

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Effects of human RelA transgene on murine macrophage inflammatory responses

Project description:The NFκB family of transcription factors is a major regulator of the innate immune responses, and its dysregulation has been linked to several inflammatory diseases. In this study we focused on bone marrow derived macrophages from the recently described p65-DsRed/IκBα-eGFP transgenic strain, in which a human copy of RelA (p65) was introduced into the mouse genome. Confocal imaging analysis showed that the human RelA is expressed these cells and can translocate to the nucleus upon Toll-like receptor 4 activation (TLR4). RNA sequencing analysis of polysaccharide-stimulated macrophage cultures, revealed that the extra copy of human RelA impacts on gene transcription, affecting both NFκB and non-NFκB target genes, including immediate-early and late response NFκB target genes, such as Fos and Cxcl10, respectively. In validation experiments on NFB targets we observed reduced mRNA levels, but similar expression kinetic profile of the transgenic cells compared to the wild type. Enrichment pathway analysis based on the differentially regulated genes revealed that interferon and cytokine signaling, are affected downstream TLR4. These immune response pathways were also affected when the macrophages were treated with tumor necrosis factor. The impact of genetic manipulation on cell-specific functions is particularly important and highlights the need of understanding the molecular basis on which complicated in vitro and in vivo experiments will be designed on.

2022-03-22 | E-MTAB-11461 | biostudies-arrayexpress

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