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The core cellular network modulates immune phenotype switching in hepatitis B

ABSTRACT: The core cellular network modulates immune phenotype switching in hepatitis B

PROVIDER: PRJNA1194020 | ENA |

REPOSITORIES: ENA

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The core cellular network modulates immune phenotype switching in hepatitis B

Project description:Hepatitis B virus (HBV) is a leading cause of liver-related diseases and mortality. However, immune mechanisms governing the phases of HBV infection remain elusive. Understanding molecular components in hepatitis immunosuppression and progression is essential for developing immunotherapies for functional cure of chronic HBV infection. Our integrative analysis of intrahepatic tissue and peripheral PBMC samples from patients with acute and chronic HBV infection using single-cell RNA sequencing (scRNA-seq) and TCR/BCR sequencing (scTCR/BCR-seq) revealed three distinct lineages of PBMC-derived intrahepatic T lymphocytes (hpCTLs): exhausted GZMK+PDCD1+, short-lived effector KLRG1+, and inactivated GZMB+PRF1+ hpCTLs. Key factors such as FasL/Fas-mediated cytotoxicity, CD28 co-stimulation, and exhaustion status were identified as determinants of hpCTL functionality. Liver-resident DC-SIGN+ macrophages were found to act as antigen-presenting cells that cross-prime hpCTLs in response to IL-2 or as suppressive macrophages by inhibiting T cell immunity through IL-10 and PD-L1 production and Treg recruitment. The intrahepatic core cellular network, including DC-SIGN+ macrophages, CSF1+ST2+ mast cells, AREG+ liver-resident NK cells, CD14+ hepatocytes, and CXCL13+ TFH, was observed to modulate immune tolerance, activation, and suppression in HBV infection. This study inferred the core cellular network involved in immune phenotype switching across different hepatitis B phases and suggested potential immunomodulatory strategies for treating chronic HBV infection.

2024-12-05 | GSE283471 | GEO

Janus kinase-Inhibition modulates hepatitis E virus infection

Project description:Janus kinase-Inhibition modulates hepatitis E virus infection

| PRJNA932725 | ENA

Transcriptome study of hepatocytes isolated from transgenic mice expressing HCV core.

Project description:Hepatitis C Virus (HCV) core protein plays a major role in HCV mediated liver pathologies. We have previously reported that HCV core variants isolated from tumoral (T) and non-tumoral (NT) livers were capable to alleviate Smad transcriptional activity and to shift TGF-β responses from tumor suppressor effects to tumor promotion. To comprehensively appreciate the consequences of core-mediated deregulation of Smad signaling on TGF-b target gene expression, Affimetrix microarrays were performed. Microarray analyses demonstrate that HCV core expression in hepatocytes modulates TGF-b target gene expression. Furthermore, most of the genes modulated in core expressing hepatocytes after TGF-b treatment were already regulated in these non treated cells suggesting that HCV core is capable to activate latent TGF-b. Transcriptome analysis was performed on primary hepatocytes from transgenic mice expressing either Core T or core NT or their control littermates treated or not with TGF-b.

2012-03-03 | E-GEOD-36220 | biostudies-arrayexpress

Transcriptome study of hepatocytes isolated from transgenic mice expressing HCV core.

2012-03-03 | GSE36220 | GEO

Hepatitis B virus core protein is not required for cccDNA transcriptional regulation

Project description:Hepatitis B virus core protein is not required for cccDNA transcriptional regulation

| PRJNA821068 | ENA

Hepatitis B virus

Project description:Hepatitis B virus preCore/Core region complexity by massive sequencing

| PRJNA260562 | ENA

mTORC1/AMPK responses define a core gene set for developmental cell fate switching

Project description:mTORC1/AMPK responses define a core gene set for developmental cell fate switching

| PRJNA509345 | ENA

CircCDYL association with hnRNPL modulates CDYL isoform switching in Breast Cancer cells

Project description:CircCDYL association with hnRNPL modulates CDYL isoform switching in Breast Cancer cells

| PRJNA1252746 | ENA

Hepatitis B Core Protein is Posttranslationally Modified through K29-linked Ubiquitination

Project description:Hepatitis B virus (HBV) core protein (HBc) plays many roles in the HBV life cycle such as regulation of transcription, RNA encapsidation, reverse transcription and viral release. To accomplish these functions, HBc interacts with many host proteins and undergoes different posttranslational modifications (PTMs). One of the most common PTM is ubiquitination that was shown to change function, stability, and intracellular localization of different viral proteins, but the role of HBc ubiquitination in the HBV life cycle remains unknown. Here, we found that HBc protein is posttranslationally modified through K29-linked ubiquitination. We performed a series of co-immunoprecipitation experiments with wild type HBc, lysine to arginine HBc mutants and wild type ubiquitin, single lysine to arginine ubiquitin mutants or single ubiquitin-accepting lysine constructs. We observed that HBc protein could be modified by ubiquitination in transfected as well as infected hepatoma cells. In addition, ubiquitination predominantly occurred on HBc lysine 7 and the preferred ubiquitin chain linkage was through ubiquitin-K29. Mass spectrometry (MS) analyses detected UBR5 as a potential E3 ubiquitin ligase involved in K29-linked ubiquitination. These findings emphasize that ubiquitination of HBc may play an important role in HBV life cycle.

2020-12-01 | PXD021712 | Pride

Vascular smooth muscle cell phenotype switching during cancer progression.

Project description:Smooth muscle cell plasticy and phenotypic switching play a prominent role in pathogenesis of multiple diseases. We used scRNAseq to look at the diversity of vascular smooth muscle cells in tumorigenesis.

2025-02-26 | GSE262942 | GEO

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