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RNA-sequencing of PD-1+ CD8 T cells following two week PD-1 blockade (stem-like and terminally-differentiated subsets).

ABSTRACT: RNA-sequencing of PD-1+ CD8 T cells following two week PD-1 blockade (stem-like and terminally-differentiated subsets).

PROVIDER: PRJNA925927 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23172800.fastq.gz	Fastqsanger.gz
	SRR23172801.fastq.gz	Fastqsanger.gz
	SRR23172802.fastq.gz	Fastqsanger.gz
	SRR23172803.fastq.gz	Fastqsanger.gz
	SRR23172804.fastq.gz	Fastqsanger.gz

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RNA-sequencing of PD-1+ CD8 T cells following two week PD-1 blockade (stem-like and terminally-differentiated subsets).

Project description:The goal of this study is to characterize the transcriptional profile of PD-1+ stem-like (Tim-3-CD73+) versus terminally-differentiated (Tim-3+CD73-) CD8 T cells following two week αPD-1 blockade.

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Novel ovarian cancer PD-1+ NK cell subsets, targetable by combined immune-checkpoint blockade

Project description:Ovarian cancer (OC) is the fifth leading cause of cancer-related death and High-Grade Serous Ovarian Carcinoma (HGSOC) is its most common histotype. Current therapies are ineffective, and most patients develop a recurrence within a few years. Moreover, if outstanding results can be obtained with immune-checkpoint blockade strategies (mainly PD-1/PD-L axis) in immunotherapeutic protocols for several aggressive tumors, clinical trials didn’t show good results with HGSOC patients so far. Here we analysed, by multiparametric flow cytometry, NK cells derived from peripheral blood, peritoneal fluid, tumor tissue, and metastatic tissue of a large cohort of HGSOC patients, in order to define how NK cells could be leveraged to improve HGSOC immunotherapy. We identified new PD-1+NK subsets occurring in HGSOC patients, but absent in healthy donors, characterized by a CD56dimNKG2A+KIR+/-NKp46+CD57low phenotype and ineffective anti-tumor response against autologous HGSOC cells. This impairment could be rescued by treatment with a combination of anti-PD-1/PD-Ls, NKG2A, and KIRs mAbs. PD-1+ NK cells were enriched in the metastatic niche and high levels of tumor-infiltrating PD-1+ NK cells correlate with a worse outcome, suggesting a role for PD-1 in metastatic promotion/progression. Our data demonstrate the existence of novel tumor-infiltrating PD-1+ NK cell subsets in HGSOC patients, which are inversely related to patient outcome, showing the importance of these NK subsets. These subsets show indeed impaired anti-tumor activity, which can be rescued by combined ICs blockade, paving the way for more successful NK cell-based immunotherapy in OC patients.

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PD-1-stimulated T cell subsets are transcriptionally and functionally distinct

Project description:Analysis of 3 subsets of primary human CD4+ T cells (naive, CM, EM) stimulated with anti-CD3, anti-CD28 and PD-L1/PD-L2 for 18 hours. we show that naive, EM, and CM T cell subsets had distinct gene expression profiles following PD-1 ligation.

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Terminally differentiated CD4+ T cells promote myocardial inflammaging

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Terminally differentiated CD4+ T cells promote myocardial inflammaging

Project description:We generated a xenograft transplantation model in which young humanized mice were treated to harbor a senescent-like human CD4+ T cell compartment. Our data uncover a role for terminally differentiated T cells in promoting cardiac inflammaging.

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Oleuropein reprograms the immunosuppressive footprint of tumor-associated myeloid cells and enhances PD-L1/PD-1 blockade immunotherapy in cancer

Project description:Therapies based on PD-1/PD-L1 blockade fail in most cancer patients. Here we evaluated the capacities of oleuropein to reprogram tumor-associated immunosuppressive myeloid cells to increase the potency of immunotherapies. Oleuropein caused major global reprogramming of monocytic and granulocytic myeloid-derived suppressor cells and tumor-associated macrophages towards immunostimulatory subsets. Differential quantitative proteomics uncovered activated and down-modulated pathways at high resolution for each subset which regulated major differentiation programs. Oleuropein significantly potentiated the capacities of myeloid cells to activate T-cells and enhanced antitumor properties of PD-1 blockade, either by systemic anti-PD-1 antibody administration, or locally by intratumor antibody delivery with a self-amplifying RNA vector based on Semliki Forest virus. Combination therapies decreased tumor infiltration by immunosuppressive myeloid cells and increased dendritic cell recruitment within draining lymph nodes, leading to systemic antitumor T-cell responses. Potent therapeutic activities were evident in lung cancer models resistant to immunotherapies and in colon cancer models.

2024-12-08 | PXD047616 | JPOST Repository

Novel ovarian cancer PD-1+ NK cell subsets, targetable by combined immune-checkpoint blockade

Project description:Novel ovarian cancer PD-1+ NK cell subsets, targetable by combined immune-checkpoint blockade

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Epigenetic signature of PD-1+ TCF1+ CD8 T cells thatact as resource cells during chronic viral infectionand respond to PD-1 blockade

Project description:We have recently defined a novel population of PD-1+TCF1+virus-specific CD8 T cells that function as resource cells during chronic LCMV infection and provide the proliferative burst seen after PD-1 blockade. Such CD8 T cells have been found in other chronic infections and also in cancer in mice and humans. These CD8 T cells exhibit stem-like properties undergoing self-renewal and also giving rise to the terminally differentiated (exhausted) CD8 T cells. Here we compared the epigenetic signature of stem-like CD8 T cells with exhausted CD8 T cells. ATAC-seq analysis showed that stem-like CD8 T cells had a unique signature implicating activity of TCF (HMG family) and NF-κB (RHD family) members. In addition, transcription factor networks including Tcf7, Id3, and Bach2 were enriched in stem-like CD8 T cells. In contrast,exhausted CD8 T cells enriched accessible sites for ETS and Runx motifs in addition to a network encompassing Prdm1 and Il10. We also compared the epigenetic signatures of the two CD8 T-cellsubsets from chronically infected mice with effector and memory CD8 T cells generated after an acute LCMV infection. Both CD8T-cell subsets generated during chronic infection were strikingly different from CD8 T-cell subsets from acute infection. Interestingly, the stem-like CD8 T-cell subset from chronic infection, despite sharing key functional properties with memory CD8 T cells,had a very distinct epigenetic program. These results show that the chronic stem-like CD8 T-cell program represents a specific adaptation of the T-cell response to persistent antigenic stimulation.

2019-06-15 | GSE132110 | GEO

Limited oxygen availability in standard cell culture alters metabolism and function in terminally differentiated cells

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Distinct cellular mechanisms underlie anti-CTLA-4 and anti-PD-1 checkpoint blockade [WES]

Project description:Immune checkpoint blockade is able to achieve durable responses in a subset of patients, however we lack a satisfying comprehension of the underlying mechanisms of anti-CTLA-4 and anti-PD-1 induced tumor rejection. To address these issues we utilized mass cytometry to comprehensively profile the effects of checkpoint blockade on tumor immune infiltrates in human melanoma and murine tumor models. These analyses reveal a spectrum of tumor infiltrating T cell populations that are highly similar between tumor models and indicate that checkpoint blockade targets only specific subsets of tumor infiltrating T cell populations. Anti-PD-1 predominantly induces the expansion of specific tumor infiltrating exhausted-like CD8 T cell subsets. In contrast, anti-CTLA-4 induces the expansion of an ICOS+ Th1-like CD4 effector population in addition to engaging specific subsets of exhausted-like CD8 T cells. Thus, our findings indicate that anti-CTLA-4 and anti-PD-1 checkpoint blockade induced immune responses are driven by distinct cellular mechanisms.

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