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TNF-receptor 2 signaling enhances suppressive abilities in human circulating T follicular regulatory cells

ABSTRACT: TNF-receptor 2 signaling enhances suppressive abilities in human circulating T follicular regulatory cells

PROVIDER: PRJNA679601 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13088300.fastq.gz	Fastqsanger.gz
	SRR13088301.fastq.gz	Fastqsanger.gz
	SRR13088302.fastq.gz	Fastqsanger.gz
	SRR13088291.fastq.gz	Fastqsanger.gz
	SRR13088292.fastq.gz	Fastqsanger.gz

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TNF-receptor 2 signaling enhances suppressive abilities in human circulating T follicular regulatory cells

Project description:Objective: T follicular regulatory (Tfr) cells express CXC chemokine receptor type 5. They migrate into germinal centers and suppress T follicular helper (Tfh) and B cells for regulating antibody production. Tumor necrosis factor (TNF) inhibitors are used in inflammatory diseases; however, autoantibody and anti-drug antibody production is challenging. As TNF receptor 2 (TNFR2) signaling is important for suppressive functions of regulatory T cells, we investigated the role of TNFR2 on Tfr cells. Methods: Tfr, Tfh, and naive B cells were obtained from human peripheral blood. Tfr cells were stimulated with MR2-1 (anti-TNFR2 agonistic antibody) and their proliferation, Forkhead box P3 (Foxp3) expression, and surface molecules were evaluated by flow cytometry. Tfh/B-cell proliferation and B-cell IgM production and differentiation in co-cultures with MR2-1-stimulated Tfr cells were examined. Results: TNFR2 expression was higher on Tfr cells than conventional T cells. MR2-1 altered the gene expression profile of Tfr cells. Cell proliferation and Foxp3 expression were induced by MR2-1. Inducible costimulator and program death-1 were dramatically upregulated in MR2-1-stimulated Tfr cells and significantly suppressed Tfh/B-cell proliferation, IgM production, and B-cell differentiation. Tfr cells treated with MR2-1 migrated according to the CXCL13 gradient. Conclusion: TNFR2 signaling in Tfr cells regulates Tfh and B-cell population. Aberrant antibody production during TNF inhibitor treatment might be associated with TNFR2 signaling inhibition in Tfr cells, suggesting TNFR1-specific inhibition as a better therapeutic strategy than pan-TNF inhibition. TNFR2-treated Tfr cells may serve as prospective candidates for cell-based therapy of autoimmune diseases.

2021-12-20 | GSE161835 | GEO

Circulating small extracellular vesicle-based miRNA classifier for follicular thyroid carcinoma: a multicenter diagnostics study

Project description:Discrimination between follicular thyroid carcinoma (FTC) and follicular thyroid adenoma (FTA) prior to surgery remains a major challenge in clinical practice. To evaluate the feasibility of circulating small extracellular vesicle (sEV)-associated and cell-free RNAs for non-invasive detection of FTC. The diagnostic properties of sEV long RNAs, cell-free long RNAs, sEV miRNAs, and cell-free miRNAs were compared for the detection of FTC.

2025-11-28 | GSE221088 | GEO

Transcriptomic profiling of circulating T follicular helper cells in kidney transplant recipients

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The cancer-suppressive tapeworm Mesocestoides corti: larval transcriptome, proteome, and functional characterization of its McKI-C1 Kunitz-type protease inhibitor

Project description:Cancer remains positioned as the leading cause of death worldwide, with nearly 10 million deaths and an estimated 20 million new cases yearly. Here, we present analyses of molecular data from the tumor-suppressing larvae of the tapeworm Mesocestoides corti, the intraperitoneal infection of which has previously demonstrated the ability to abrogate the growth and metastasis of the highly aggressive B16F10 melanoma in mice. In order to explore the potential effector mechanisms and molecules behind its cancer-suppressive capabilities, we analyzed the M. corti larval transcriptome in the C57BL/6J and ICR mouse strains, as well as in vitro, and the proteomic profiles of whole worm homogenate and its excretory-secretory products. We present, thus far, the most extensive list of experimentally verified M. corti protein products. These were searched for molecules potentially responsible for the tapeworm’s immune-related cancer-suppressive abilities. Many proteins with potential immunomodulatory properties were found within its proteome, including those from the cysteine-rich secretory CAP family, such as GLIPR-like proteins. Furthermore, functional tests of McKI-C1, an ortholog of the anti-cancer Kunitz inhibitor EgKI-1 from Echinococcus granulosus, were performed both in vitro and in vivo, to ascertain whether it could express a similar effect. While McKI-C1 did not show itself as an effector molecule in the tapeworm’s cancer-suppressive abilities, the extensive list of potentially functional molecules prompts further exploration.

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Change in circulating miRNA at two weeks after anti-TNF therapy predicts response at 14 weeks: a pilot study

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Pleiotropic tumor suppressive functions of PTEN missense mutations during gliomagenesis

Project description:PTEN plays a crucial role in preventing the development of glioblastoma (GBM), a severe and untreatable brain cancer. In GBM, most PTEN deficiencies arise from missense mutations, many of which have not been thoroughly examined. Here, we leveraged genetically modified mice and matched isogenic astrocyte cell cultures to investigate how specific and clinically relevant PTEN mutations (G36E, L42R, C105F, and R173H) behave in the development of GBM driven by EGFR. We report that the tumor-suppressive abilities of these PTEN mutants do not depend on their ability to act as lipid phosphatases but are instead related to their increased presence at the cell membrane. Moreover, these PTEN mutations led to heightened EGFR activity by keeping EGFR within endomembranes longer, affecting its signaling behavior. Through comprehensive studies on global protein phosphorylation and kinase library analyses in cells with the G36E and L42R PTEN mutations, we identified distinct cancer-promoting pathways activated by EGFR, offering new targets for treating GBM with these PTEN alterations.

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Autonomous TNF is critical for monocyte survival in steady state and inflammation in vivo

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