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CTLA4 limits expansion of human cytotoxic CD4+ T cells to prevent B cell apoptosis

ABSTRACT: CTLA4 limits expansion of human cytotoxic CD4+ T cells to prevent B cell apoptosis

PROVIDER: PRJNA718290 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14095380.fastq.gz	Fastqsanger.gz
	SRR14095381.fastq.gz	Fastqsanger.gz
	SRR14095382.fastq.gz	Fastqsanger.gz
	SRR14095383.fastq.gz	Fastqsanger.gz
	SRR14095384.fastq.gz	Fastqsanger.gz

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CTLA4 limits expansion of human cytotoxic CD4+ T cells to prevent B cell apoptosis

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Expression data from Ctla4-/- and DKO CD4+ Tconv cells

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A MYC/GCN2/eIF2alpha negative feedback loop limits protein synthesis to prevent MYC-dependent apoptosis in colorectal cancer

Project description:A MYC/GCN2/eIF2alpha negative feedback loop limits protein synthesis to prevent MYC-dependent apoptosis in colorectal cancer

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Functional characterization of human T cell hyporesponsiveness induced by CTLA4-Ig

Project description:During activation, T cells integrate multiple signals from APCs and cytokine milieu. The blockade of these signals can have clinical benefits as exemplified by CTLA4-Ig, which blocks interaction of B7 co-stimulatory molecules on APCs with CD28 on T cells. Variants of CTLA4-Ig, abatacept and belatacept are FDA approved as immunosuppressive agents in arthritis and transplantation whereas murine studies suggested that CTLA4-Ig can be beneficial in a number of other diseases. However, detailed analysis of human CD4 cell hyporesponsivness induced by CTLA4-Ig has not been performed. Herein, we established a model to study effect of CTLA4-Ig on the activation of human naM-CM-/ve T cells in a human mixed lymphocytes system. Comparison of human CD4 cells activated in the presence or absence of CTLA4-Ig, showed that co-stimulation blockade during TCR activation does not affect NFAT signaling but results in decreased activation of NF-kB and AP-1 transcription factors followed by profound decrease in proliferation and cytokine production. The resulting T cells become hyporesponsive to secondary activation and, although capable of receiving TCR signals, fail to proliferate or produce cytokines, demonstrating properties of anergic cells. However, unlike some models of T cell anergy, these cells did not possess increased levels of TCR signaling inhibitor CBLB. Rather, the CTLA4-Ig induced hyporesponsiveness was associated with an elevated level of p27kip1 cyclin-dependent kinase inhibitor. Time series. Human resting and activated T cell dUTP mRNA-Seq profiles were generated on Illumina HiSeq2500

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CD39+ CD4+ conventional T cells with exhaustion traits and cytotoxic potential infiltrate tumors and expand upon CTLA4 blockade

Project description:CD39+ CD4+ conventional T cells with exhaustion traits and cytotoxic potential infiltrate tumors and expand upon CTLA4 blockade

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Functional characterization of human T cell hyporesponsiveness induced by CTLA4-Ig

Project description:During activation, T cells integrate multiple signals from APCs and cytokine milieu. The blockade of these signals can have clinical benefits as exemplified by CTLA4-Ig, which blocks interaction of B7 co-stimulatory molecules on APCs with CD28 on T cells. Variants of CTLA4-Ig, abatacept and belatacept are FDA approved as immunosuppressive agents in arthritis and transplantation whereas murine studies suggested that CTLA4-Ig can be beneficial in a number of other diseases. However, detailed analysis of human CD4 cell hyporesponsivness induced by CTLA4-Ig has not been performed. Herein, we established a model to study effect of CTLA4-Ig on the activation of human naïve T cells in a human mixed lymphocytes system. Comparison of human CD4 cells activated in the presence or absence of CTLA4-Ig, showed that co-stimulation blockade during TCR activation does not affect NFAT signaling but results in decreased activation of NF-kB and AP-1 transcription factors followed by profound decrease in proliferation and cytokine production. The resulting T cells become hyporesponsive to secondary activation and, although capable of receiving TCR signals, fail to proliferate or produce cytokines, demonstrating properties of anergic cells. However, unlike some models of T cell anergy, these cells did not possess increased levels of TCR signaling inhibitor CBLB. Rather, the CTLA4-Ig induced hyporesponsiveness was associated with an elevated level of p27kip1 cyclin-dependent kinase inhibitor.

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Expression data from Ctla4-/- and DKO CD4+ Tconv cells

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CTLA4-Ig changed the gene expression associated with cellular movement in osteoclast precursors

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