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

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

PROVIDER: PRJNA494812 | ENA |

REPOSITORIES: ENA

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

Project description:Bcl11b binding and 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

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

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Genome wide mapping in regulatory T cells at steady state

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