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Bcl11b binding and transcriptome analysis of Bcl11b-deficient MAIT cells at steady state and infection

ABSTRACT: Bcl11b binding and transcriptome analysis of Bcl11b-deficient MAIT cells at steady state and infection

PROVIDER: PRJNA608197 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11149251_1.fastq.gz	Fastqsanger.gz
	SRR11149251_2.fastq.gz	Fastqsanger.gz
	SRR11149252_1.fastq.gz	Fastqsanger.gz
	SRR11149252_2.fastq.gz	Fastqsanger.gz
	SRR11149253_1.fastq.gz	Fastqsanger.gz

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Transcriptome analysis of Bcl11b-deficient MAIT cells at steady state and infection

Project description:Transcriptome analysis of Bcl11b-deficient MAIT cells at steady state and infection

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Transcriptome analysis of Bcl11b-deficient MAIT cells at steady state and infection

Project description:Mucosal associated invariant T (MAIT) cells, already differentiated and located at mucosal sites, are critical in the body’s first wave of defenses against invading pathogens. Bcl11b KO MAIT cells fail to be maintained both in the thymus and peripheral organs. Furthermore, MAIT cells fail to fully develop in the thymus without Bcl11b, failing to upregulate RORγt, and that phenotype remains in the lungs and livers of these mice. Bcl11b deletion in MAIT cells causes dramatic shifts in the activation and TH17 programs, due to the binding of Bcl11b in many of those genes, which we have seen in the human MAIT cells. MAIT cells rely on PLZF and RORγt for their development and function, while also heavily relying on Bcl11b. These data show the key interplay of Bcl11b with PLZF and RORγt in a T cell leading to its development and necessary function to protect the body against diseases.

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Transcriptome analysis of Bcl11b-deficient regulatory T cells at steady state

Project description:T regulatory (Treg) cells have been studied in depth since their discovery for their potential use in therapies of autoimmune diseases. Treg cells have a suppression program that includes surface molecules CD25 (IL2R), cytotoxic T-lymphocyte associated protein 4 (CTLA4), and glucocorticoid-induced TNFR family (GITR) to limit aberrant and excessive inflammatory immune responses. We have shown that Bcl11b can bind to the CNS2 region in Foxp3 as well as the gene loci of those essential surface molecules for Treg suppression. Furthermore, we have identified a subset of Foxp3-independent genes in Treg cells directly regulated by Bcl11b binding. Bcl11b also directly represses expression of innate molecules such as transcription factors PU.1 and ID2 in Treg cells. Finally, we have also shown that removal of Bcl11b accelerates apoptosis in Treg cells as cleaved caspase 3 levels were significantly elevated in Bcl11b KO Treg cells when compared with WT Treg cells.

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Mapping Bcl11b binding in human MAIT cells

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Expression profile of bcl11b-deficient NAÏVE CD8+ T cells versus wild type

Project description:Naïve CD44low CD25low CD8+ T cells from Bcl11bF/F/dLck-iCre and wild type mice at steady state were sorted at 90% purity, RNA was extracted and profile for mRNA expression to identify mRNAs differentially expressed in Bcl11b-/- naïve CD8+ T cells versus wild type. Naïve CD44low CD25low CD8+ T cells purified from Bcl11bF/F/dLck-iCre and wild type mice and investigated for mRNA expression

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Mouse iNKT cell: Wild type Vs Bcl11b deficient

Project description:Transcriptional profiling of mouse iNKT cells comparing wild type and Bcl11b deficient cell. The mice were treated with 4 Î¼g of Î±-galactosylceramide. Goal was to determine the effects of transcription factor Bcl11b removal in iNKT cells. Intraperitoneal treatment with 4 Î¼g of Î±-Galactosylceramide. Two pair of wild type (BCL11b F/F VÎ±14 transgenic) and Knock out (BCL11b F/F PLZF-Cre VÎ±14 transgenic)) mice were treated. Lymphocytes from spleen and liver were enriched and stain with PBS-57 Loaded CD1d tetramer. Pure iNKT cells were collected through cell sorter.

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Bcl11b binding and transcriptome analysis of Bcl11b-deficient MAIT cells at steady state and infection

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-03-22 | GSE145779 | GEO