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The expression of MHC class II molecules on murine breast tumors delays T cell exhaustion, expands the T cell repertoire and slows tumor growth

ABSTRACT: The expression of MHC class II molecules on murine breast tumors delays T cell exhaustion, expands the T cell repertoire and slows tumor growth

PROVIDER: PRJNA489881 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7807460_1.fastq.gz	Fastqsanger.gz
	SRR7807460_2.fastq.gz	Fastqsanger.gz
	SRR7807461_1.fastq.gz	Fastqsanger.gz
	SRR7807461_2.fastq.gz	Fastqsanger.gz

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The expression of MHC class II molecules on murine breast tumors delays T-cell exhaustion, expands the T-cell repertoire, and slows tumor growth.

Project description:The expression of MHC class II molecules (MHCII) on tumor cells correlates with survival and responsiveness to immunotherapy. However, the mechanisms underlying these observations are poorly defined. Using a murine breast tumor line, we showed that MHCII-expressing tumors grew more slowly than controls and recruited more functional CD4+ and CD8+ T cells. In addition, MHCII-expressing tumors contained more TCR clonotypes expanded to a larger degree than control tumors. Functional CD8+ T cells in tumors depended on CD4+ T cells. However, both CD4+ and CD8+ T cells eventually became exhausted, even in MHCII-expressing tumors. Treatment with anti-CTLA4, but not anti-PD-1 or anti-TIM-3, promoted complete eradication of MHCII-expressing tumors. These results suggest tumor cell expression of MHCII facilitates the local activation of CD4+ T cells, indirectly helps the activation and expansion of CD8+ T cells, and, in combination with the appropriate checkpoint inhibitor, promotes tumor regression.

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The expression of MHC class II molecules on murine breast tumors delays T cell exhaustion, expands the T cell repertoire and slows tumor growth

Project description:Transfection with the human class II transcriptional activator (hCIITA) promotes MHCII expression on TS/A breast cancer cells. Using a murine breast tumor line, we showed that MHCII-expressing tumors grew more slowly than controls and recruited more functional CD4+ and CD8+ T cells. Additionally, MHCII-expressing tumors contained more TCR clonotypes expanded to a larger degree than control tumors. Functional CD8+ T cells in tumors depended on CD4+ T cells. However, both CD4+ and CD8+ T cells eventually became exhausted, even in MHCII-expressing tumors. Treatment with anti-CTLA4, but not anti-PD-1 or anti-TIM-3, promoted complete eradication of MHCII-expressing tumors. These results suggest tumor cell expression of MHCII facilitates the local activation of CD4+ T cells, indirectly helps the activation and expansion of CD8+ T cells and, in combination with the appropriate checkpoint inhibitor, promotes tumor regression.

2018-09-08 | GSE119670 | GEO

Attenuation of miR-126 activity expands HSC in vivo without exhaustion

Project description:Life-long blood cell production is governed through the poorly understood integration of cell-intrinsic and -extrinsic control of hematopoietic stem cell (HSC) quiescence and activation. MicroRNAs (miRNAs) coordinately regulate multiple targets within signaling networks making them attractive candidate HSC regulators. We report that miR-126, a miRNA expressed in HSC and early progenitors, plays a pivotal role in restraining cell cycle progression of HSC in vitro and in vivo. miR-126 knockdown using lentiviral sponges increased HSC proliferation without inducing exhaustion, resulting in expansion of mouse and human long-term repopulating HSC. Conversely, enforced miR-126 expression impaired cell cycle entry leading to progressively reduced hematopoietic contribution. In HSC/early progenitors, miR-126 regulates multiple targets within the PI3K/AKT/GSK3β pathway thus attenuating signal transduction in response to extrinsic signals. These data establish that miR-126 sets a threshold for HSC activation and thus governs HSC pool size, demonstrating the importance of miRNA in the control of HSC function. Total RNA was extracted from cord blood Lin- cells and treated with mir126 shRNA or mir126 containing viral particles (and corresponding controls)

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Multiomic profiling of chronically activated CD4+ T cells identifies drivers of exhaustion and metabolic reprogramming

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3’ Uridylation Expands miRNA Target Repertoire

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Transcriptome differences in HCC infiltrated CD8+ T cells in effector and exhaustion state

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