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Circulating monocytes associated with anti-PD-1 resistance in human biliary cancer induce T cell paralysis

ABSTRACT: Circulating monocytes associated with anti-PD-1 resistance in human biliary cancer induce T cell paralysis

PROVIDER: PRJNA863602 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20711275_1.fastq.gz	Fastqsanger.gz
	SRR20711275_2.fastq.gz	Fastqsanger.gz
	SRR20711276_1.fastq.gz	Fastqsanger.gz
	SRR20711276_2.fastq.gz	Fastqsanger.gz
	SRR20711277_1.fastq.gz	Fastqsanger.gz

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Circulating monocytes associated with anti-PD-1 resistance in human biliary cancer induce T cell paralysis [scRNA-seq]

Project description:Suppressive myeloid cells can contribute to immunotherapy resistance, but their role in response to checkpoint inhibition (CPI) in anti-PD-1 refractory cancers, such as biliary tract cancer (BTC), is largely unknown. We use multiplexed single-cell transcriptomic and epitope sequencing to profile greater than 200,000 peripheral blood mononuclear cells from advanced BTC patients (n=9) and matched healthy donors (n=8). Following anti-PD-1 treatment, CD14+ monocytes expressing high levels of immunosuppressive cytokines and chemotactic molecules (CD14CTX) increase in the circulation of patients with BTC tumors that are CPI-resistant. CD14CTX can directly suppress CD4+ T cells and induce SOCS3 expression in CD4+ T cells rendering them functionally unresponsive. The CD14CTX gene signature associates with worse survival in patients with BTC as well as in other anti-PD-1 refractory cancers. These results demonstrate that monocytes arising after anti-PD-1 treatment can induce T cell paralysis as a distinct mode of tumor-mediated immunosuppression leading to CPI resistance.

2022-08-01 | GSE210066 | GEO

Circulating monocytes associated with anti-PD-1 resistance in human biliary cancer induce T cell paralysis [CITE-seq]

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Circulating monocytes associated with anti-PD-1 resistance in human biliary cancer induce T cell paralysis [bulkRNA-seq]

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Circulating monocytes associated with anti-PD-1 resistance in human biliary cancer induce T cell paralysis [CITE-seq]

Project description:Circulating monocytes associated with anti-PD-1 resistance in human biliary cancer induce T cell paralysis [CITE-seq]

| PRJNA863605 | ENA

Circulating monocytes associated with anti-PD-1 resistance in human biliary cancer induce T cell paralysis [scRNA-seq]

Project description:Circulating monocytes associated with anti-PD-1 resistance in human biliary cancer induce T cell paralysis [scRNA-seq]

| PRJNA863606 | ENA

Circulating monocytes associated with anti-PD-1 resistance in human biliary cancer induce T cell paralysis [bulkRNA-seq]

Project description:Circulating monocytes associated with anti-PD-1 resistance in human biliary cancer induce T cell paralysis [bulkRNA-seq]

| PRJNA872401 | ENA

Circulating monocytes associated with anti-PD-1 resistance in human biliary cancer induce T cell paralysis.

Project description:Suppressive myeloid cells can contribute to immunotherapy resistance, but their role in response to checkpoint inhibition (CPI) in anti-PD-1 refractory cancers, such as biliary tract cancer (BTC), remains elusive. We use multiplexed single-cell transcriptomic and epitope sequencing to profile greater than 200,000 peripheral blood mononuclear cells from advanced BTC patients (n = 9) and matched healthy donors (n = 8). Following anti-PD-1 treatment, CD14+ monocytes expressing high levels of immunosuppressive cytokines and chemotactic molecules (CD14CTX) increase in the circulation of patients with BTC tumors that are CPI resistant. CD14CTX can directly suppress CD4+ T cells and induce SOCS3 expression in CD4+ T cells, rendering them functionally unresponsive. The CD14CTX gene signature associates with worse survival in patients with BTC as well as in other anti-PD-1 refractory cancers. These results demonstrate that monocytes arising after anti-PD-1 treatment can induce T cell paralysis as a distinct mode of tumor-mediated immunosuppression leading to CPI resistance.

| S-EPMC10060099 | biostudies-literature

Circulating monocytes associated with anti-PD-1 resistance in human biliary cancer induce T cell paralysis

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

2022-08-01 | GSE210067 | GEO

Circulating exosomal microRNAs are indicative of patients with biliary colic

Project description:Background: Gallstone disease (GSD) is one of the most prevalent and costly digestive system diseases in the world and can lead to pancreatitis, severe biliary tract infection and malignant biliary tract tumors. Gallstones can induce biliary colic, and the pain radiates to the shoulder and back. Severe attacks cause nausea and vomiting, which seriously affect the patient's work and life. Exosomes are important extracellular vesicles, and exosomal microRNAs (miRNAs) can be used as biomarkers and therapeutic targets for a variety of diseases. To the best of our knowledge, exosomal miRNA has not been well evaluated as a biomarker of the progression of cholelithiasis or the onset of biliary colic. Methods: Plasma samples from 10 patients with biliary colic attack were collected for exosome extraction, identification and miRNA sequencing. The exosome miRNA sequencing data of 10 healthy people in the GEO database were used as controls for data analysis. Results: Comparison of the plasma exosomal miRNAs of patients with biliary colic to those of healthy controls showed that 35 exosomal miRNAs were upregulated and 9 miRNAs were downregulated. GO and KEGG analyses showed that differential miRNAs are involved in the inflammatory response. The analysis of the subject operation characteristic curve shows that the expression of plasma exosomal miR-1268a can better reflect the attack characteristics of biliary colic than other miRNAs. miR-146a-3p participates in body inflammation and lipid metabolism processes and can be used as a potential therapeutic target. Conclusion: Plasma exosomal miRNAs can be used as biomarkers during the onset of biliary colic and can also be used as potential molecular targets to inhibit inflammation and analgesia.

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