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Pro-tumor Tfh2 cells induce detrimental IgG4 production and PGE2-dependent IgE inhibition in pancreatic cancer (tfh)

ABSTRACT: Pro-tumor Tfh2 cells induce detrimental IgG4 production and PGE2-dependent IgE inhibition in pancreatic cancer (tfh)

PROVIDER: PRJNA1015281 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26033900.fastq.gz	Fastqsanger.gz
	SRR26033901.fastq.gz	Fastqsanger.gz
	SRR26033902.fastq.gz	Fastqsanger.gz
	SRR26033903.fastq.gz	Fastqsanger.gz
	SRR26033904.fastq.gz	Fastqsanger.gz

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Pro-tumor Tfh2 cells induce detrimental IgG4 production and PGE2-dependent IgE inhibition in pancreatic cancer (tfh)

Project description:Background: Pancreatic ductal adenocarcinoma (PDAC) has a dismal prognosis and it is characterized by predominant pro-tumor Th2-type inflammation. T follicular helper (Tfh) cells are relevant immunoregulators in cancer, and often correlate with better survival. How the Th2-skewed microenvironment in PDAC modulates the differentiation of Tfh cells and their immunoregulatory function is unknown. Methods: We carried out high-dimensional flow cytometry and T-cell receptor- and RNA-sequencing, as well as bioinformatics, immunohistochemistry and in vitro mechanistic studies. Findings: We identified Tfh1-, Tfh2-, and Tfh17-like cell clusters in the blood, tumors and tumor draining lymph-nodes (TDLNs) of chemo-naïve PDAC patients and showed that high percentages of Tfh2 cells within the tumor tissue and TDLNs correlated with reduced patient survival. Moreover, only Tfh2 cells were highly activated and were reduced in frequency in patients who responded to neoadjuvant chemotherapy. RNA-sequencing analysis of immunoglobulin expression showed that tumor and TDLN samples expressed all immunoglobulin (IGH) isotypes apart from IGHE. Consistent with these findings, Tfh2 cells differentiated in vitro by tumor microenvironment-conditioned dendritic cells promoted the production of anti-inflammatory IgG4 antibodies by co-cultured B cells, dependent on IL-13. Moreover, unexpectedly, Tfh2 cells inhibited the secretion of pro-inflammatory IgE, dependent on prostaglandin E2. Interpretation: Our results indicate that in PDAC, highly activated pro-tumor Tfh2 favor anti-inflammatory IgG4 production, while inhibit pro-inflammatory IgE. Thus, targeting the circuits that drive Tfh2 cells, in combination with chemotherapy, may re-establish beneficial anti-tumor Tfh–B cell interactions and facilitate more effective treatment.

2023-10-04 | GSE242916 | GEO

Pro-tumor Tfh2 cells induce detrimental IgG4 production and PGE2-dependent IgE inhibition in pancreatic cancer (tumor)

2023-10-04 | GSE242915 | GEO

Pro-tumor Tfh2 cells induce detrimental IgG4 production and PGE2-dependent IgE inhibition in pancreatic cancer

Project description:Pro-tumor Tfh2 cells induce detrimental IgG4 production and PGE2-dependent IgE inhibition in pancreatic cancer

| PRJNA1015278 | ENA

Pro-tumor Tfh2 cells induce detrimental IgG4 production and PGE2-dependent IgE inhibition in pancreatic cancer (tumor)

Project description:Pro-tumor Tfh2 cells induce detrimental IgG4 production and PGE2-dependent IgE inhibition in pancreatic cancer (tumor)

| PRJNA1015280 | ENA

Gene expression of Tfh cells in the lessions of IgG4-related disease.

Project description:To address a possible role of Tfh (CD3+CD4+CXCR5hiPD-1hi) cells in IgG4-related disease(IgG4-RD), we investigated Tfh cells as well as other lymphocyte subsets residing within the affected tissue lesions of IgG4-RD in this study. When compared to gene expression profiles of Tfh cells within tonsils, inflammatory lesions in IgG4-RD preferentially contained Tfh cells with the expression of signature genes of cytotoxic T lymphocytes. Whereas the expression levels of Tfh-related genes like IL-21, CD200, and Pou2af1 (also named as Bob1) in GC-type Tfh cells of IgG4-RD seemed to be relatively lower than those of GC-type Tfh cells within tonsils. GC-type Tfh cells of IgG4-RD expressed low levels of genes related to Th2 cells, Th17 cells, and Treg cells, albeit the genes related to Th1 cells and interaction of T cells and B cells.

2022-08-10 | GSE202615 | GEO

Gene expression of CD4+CD8+ Tfh cells in lesions of IgG4-related disease and CD4+CD8+ Tfh in tonsil.

Project description:To further know features of CD4+CD8+ Double positive (DP)-Tfh cells in respective lymphoid tissues, we subsequently investigated transcriptomes of DP-Tfh cells in submandibular gland lesions of IgG4-RD in comparison to those of DP-Tfh cells in tonsils. Results showed that DP-Tfh cells of IgG4-RD lesions were more apt to present CTL-related genes such as Eomes and granzymes than DP-Tfh cells in tonsils. It was also noted that the level of CD70 in DP-Tfh cells of IgG4-RD lesions was higher than that of tonsillar DP-Tfh cells. Genes related to Tfh cell function were seemed to be presented in DP-Tfh cells of tonsils compared to DP-Tfh cells of IgG4-RD lesions.

2022-08-10 | GSE202617 | GEO

Pro-tumor Tfh2 cells induce detrimental IgG4 production and PGE2-dependent IgE inhibition in pancreatic cancer

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

2023-10-04 | GSE242917 | GEO

Gene expression of Tfh cells in the lessions of IgG4-related disease.

Project description:Gene expression of Tfh cells in the lessions of IgG4-related disease.

| PRJNA836781 | ENA

Gene expression of CD4+CD8+ Tfh cells in lesions of IgG4-related disease and CD4+CD8+ Tfh in tonsil.

Project description:Gene expression of CD4+CD8+ Tfh cells in lesions of IgG4-related disease and CD4+CD8+ Tfh in tonsil.

| PRJNA836785 | ENA

PGE2 effect on unstimulated and exhausted human CD8+ T-cells

Project description:Prostaglandin E2 (PGE2) is overexpressed in many tumors and plays an important role in suppressing T-cell function. In this study, we investigated the effect of PGE2 in human T-cells. Importantly, PGE2 caused profound transcriptomic changes both in unstimulated and exhausted T-cells with many genes and pathways altered including T-cell lipid metabolism. Our study suggests that PGE2-induced metabolic reprogramming is detrimental to dysfunctional T-cells and TIL, and its manipulation could be used to dampen the immunosuppressive effects of PGE2.

2024-03-08 | GSE227316 | GEO

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