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Immune response of TRIM28 KO cells infected with H5N1 HPAIV

ABSTRACT: Immune response of TRIM28 KO cells infected with H5N1 HPAIV

PROVIDER: PRJNA851811 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19786452_1.fastq.gz	Fastqsanger.gz
	SRR19786452_2.fastq.gz	Fastqsanger.gz
	SRR19786453_1.fastq.gz	Fastqsanger.gz
	SRR19786453_2.fastq.gz	Fastqsanger.gz
	SRR19786454_1.fastq.gz	Fastqsanger.gz

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Immune response of TRIM28 KO cells infected with H1N1 IAV

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Immune response of TRIM28 KO cells infected with H1N1 IAV

Project description:Immune response of TRIM28 KO cells infected with H1N1 IAV

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Immune response of TRIM28 KO cells infected with H5N1 HPAIV

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RNA-seq of gonadal adipose tissue from male and female Trim28-WT and Trim28 adipose specific KO mice

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Comparison of gene expression in Wild type and T cell-specific conditional Trim28 KO in TCR stimulated and un-stimulated naive CD4 positive and T regulatory cells

Project description:A microarray study was performed in unstimulated and TCR-stimulated CD4 + T cells and Treg in wild type and conditional Trim28 KO mice to identify genes that are regulated by Trim28. These experiments constitute a portion of the study described below: Paper Abstract: Peripheral T cell activation and differentiation into specialized effectors are regulated by TCR- and cytokine-mediated signals that induce clonal expansion and unique transcriptional factors. These processes may include active chromatin modification by nuclear factors. In search of such molecules, we found Trim28, a component of large nuclear chromatin-regulatory complex is tightly controlled upon TCR stimulation at the level of phosphorylation, and examined global impact of Trim28 loss in especially CD4+ T cells, by generating T cell-specific conditional Trim28 KO mice (CKO). CD4+ T cells from CKO mice showed defective IL-2 production and T cell proliferation associated with defective upregulation of cell-cycle associated proteins. Accordingly, young CKO showed T-lymphopenia. Surprisingly, Trim28 CKO mice eventually accumulated auto-reactive memory-phenotype T cells that produced inflammatory IL-17. CKO mice are also susceptible to induced auto-inflammatory disease with TH-17 dominant immune response. Loss of Trim28 showed aberrant accumulation of TH-17 and FoxP3+ T cells, two key T cells in inflammation vs. tolerance. We found CKO T cells showed a cell-extrinsic promotion of TH-17 and FoxP3+ T cell development by a mechanism involving overproduction of TGF-beta. Our study revealed unexpected roles of Trim28, a global chromatin regulator in both T cell activation and tolerance. Trim28 conditional KO mice and age-matched control mice were sacrificed, and neive CD4+ T cells (CD4+CD62+CD25-) and Treg (CD4+CD62+CD25+) were sorted. Stimulation of naive T cells was done with anti-CD3 and anti-CD28 for 13 hours. We collected quadruplicates for each group.

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