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Therapeutic vaccine induced plasma cell differentiation is defective upon persistent HBsAg stimulation [bulkRNA]

ABSTRACT: Therapeutic vaccine induced plasma cell differentiation is defective upon persistent HBsAg stimulation [bulkRNA]

PROVIDER: PRJNA962879 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24339331_1.fastq.gz	Fastqsanger.gz
	SRR24339331_2.fastq.gz	Fastqsanger.gz
	SRR24339332_1.fastq.gz	Fastqsanger.gz
	SRR24339332_2.fastq.gz	Fastqsanger.gz
	SRR24339333_1.fastq.gz	Fastqsanger.gz

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Therapeutic vaccine induced plasma cell differentiation is defective upon persistent HBsAg stimulation [bulkRNA]

Project description:Background & Aims: The precise mechanism underlying the attenuation of the antigen-specific B cell response induced by therapeutic vaccination during chronic HBV infection remains unclear. The development of vaccines or strategies targeting this impediment through rational design could potentially result in significant advancements in the treatment of chronic hepatitis B. Methods: A mouse model with a knock-in of a B cell receptor specific to the hepatitis B virus surface antigen was generated under the name E6F6-B. This model was utilized to investigate the temporal and spatial patterns of humoral responses induced by therapeutic vaccination in the presence of persistent antigen stimulation. Through the use of multiple transcriptome sequencing techniques, the differentiation trajectory of HBsAg-specific B cells post therapeutic vaccination during chronic hepatitis B infection was elucidated. Results: In light of the E6F6-B transfer model, a significant reduction in antibody secreting cells were observed two weeks after vaccination. Additionally, an atypical pre-plasma cell population (BLIMP-1+ IRF4+ CD40- CD138-) was identified as a consequence of persistent BCR signaling in the absence of CD40 co-stimulation. A therapeutic antibody-induced suppression of BCR signaling revitalized the HBsAg-specific B cell response.

2024-04-28 | GSE230861 | GEO

Therapeutic vaccine induced plasma cell differentiation is defective upon persistent HBsAg stimulation

Project description:Therapeutic vaccine induced plasma cell differentiation is defective upon persistent HBsAg stimulation

| PRJNA962873 | ENA

Therapeutic vaccine induced plasma cell differentiation is defective upon persistent HBsAg stimulation [scRNA]

2024-04-28 | GSE230862 | GEO

Therapeutic vaccine induced plasma cell differentiation is defective upon persistent HBsAg stimulation [scRNA]

Project description:Therapeutic vaccine induced plasma cell differentiation is defective upon persistent HBsAg stimulation [scRNA]

| PRJNA962880 | ENA

Therapeutic vaccine induced plasma cell differentiation is defective upon persistent HBsAg stimulation

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

2024-04-28 | GSE230863 | GEO

Transcription profiling of human HepG2 cells transfected with HBsAG to investigate the global exploration of interaction between HBsAg expression and hepatocytes

Project description:In patient serum, HBsAg particles can outnumber HBV particles by 1000:1 or higher. To explore the interactions between HBsAg and hepatocytes, concentrating on the possible effects of persistently secreting HBsAg on the functions of host cells, we have used the S gene of a full-length HBV isolate derived from an HBsAg chronic carrier (code No. C8, GenBank accession No. AF461363), cloned into pCMV vector to transfect HepG2 cells. G418 resistant clones secreting HBsAg were selected to establish permanent cell lines, and control clones transfected only with the vector were passaged as well to serve as controls. Cells were separately collected on the fourth and the eighth day after seeding, and gene expression profiles of both cell clones were studied and compared by microarray. Totally, 340 genes were suppressed and 673 genes were induced by the expression of HBsAg on the fourth day, whereas 219 genes were down-regulated and 683 genes were up-regulated on the eighth day. Arbitrarily, changes of genes detected on both 4th and 8th day cultures were selected for further study. Many cellular functions such as immune response, xenobiotic metabolism, ubiquitin pathway, transcription regulation were affected by HBsAg expression, indicating a close association between HBsAg and host cells. Experiment Overall Design: HBsAg particles are composed of viral envelope proteins and outnumber HBV virions by 1000:1 or even higher. This unique characteristic of HBV remains to be one of the challenges in basic and clinical aspects of viral hepatitis B. Experiment Overall Design: In this study, we want to explore the interactions between HBsAg and hepatocytes, concentrating on the effects of persistently secreting HBsAg on host cell functions.

2008-06-13 | E-GEOD-4549 | biostudies-arrayexpress

Global exploration of interaction between HBsAg expression and Hepatocytes

Project description:In patient serum, HBsAg particles can outnumber HBV particles by 1000:1 or higher. To explore the interactions between HBsAg and hepatocytes, concentrating on the possible effects of persistently secreting HBsAg on the functions of host cells, we have used the S gene of a full-length HBV isolate derived from an HBsAg chronic carrier (code No. C8, GenBank accession No. AF461363), cloned into pCMV vector to transfect HepG2 cells. G418 resistant clones secreting HBsAg were selected to establish permanent cell lines, and control clones transfected only with the vector were passaged as well to serve as controls. Cells were separately collected on the fourth and the eighth day after seeding, and gene expression profiles of both cell clones were studied and compared by microarray. Totally, 340 genes were suppressed and 673 genes were induced by the expression of HBsAg on the fourth day, whereas 219 genes were down-regulated and 683 genes were up-regulated on the eighth day. Arbitrarily, changes of genes detected on both 4th and 8th day cultures were selected for further study. Many cellular functions such as immune response, xenobiotic metabolism, ubiquitin pathway, transcription regulation were affected by HBsAg expression, indicating a close association between HBsAg and host cells. Keywords: interaction, HBsAg expression, hepatocyte function

2006-03-28 | GSE4549 | GEO

Association of HBsAg levels with differential gene expression in NK, CD8 T, and memory B cells in treated patients with chronic HBV

Project description:Hepatitis B surface antigen (HBsAg) secretion may impact the immune response in chronic hepatitis B virus (HBV) infection. Therapeutic approaches to suppress HBsAg production are being investigated. Our study aims to examine the immunomodulatory effects of high and low levels of circulating HBsAg by analyzing single-cell RNA sequencing data (scRNAseq) from blood and liver fine-needle aspirates (FNA). This will help to better understand anti-HBV immunity.

2024-01-01 | GSE247322 | GEO

Analysis of differentially expressed genes in intrahepatic HBsAg accumulating mice

Project description:Search for distinct genes whose expression correlates with IFN⍺ mediated liver injury in HBsAg-Tg mice. IFN treatment induces liver injury from 8 hours post IFN treament, peaking at 24 hours, in HBs transgenic mice and not in the non-transgenic (control) mice

2019-10-16 | GSE138916 | GEO

Spatial transcriptomics reveals a low extent of transcriptionally active hepatitis B virus integration in patients with HBsAg loss

Project description:Hepatitis B virus (HBV) can integrate into the chromosomes of infected hepatocytes, contributing to the production of hepatitis B surface antigen (HBsAg) and to hepatocarcinogenesis. We performed spatial transcriptomics to investigate the intrahepatic cell heterogeneity and the spatial distribution of transcriptionally active HBV integration events in different phases of chronic HBV infection. Our analysis revealed that transcriptionally active HBV integration occurred in chronically HBV-infected patients in different phases, including those patients with HBsAg loss, and antiviral treatment was associated with a decreased number and extent of viral integrations.

2023-09-30 | GSE243367 | GEO

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