Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The immune landscape and mechanism of hepatitis B virus surface antigen clearance [CITEseq]

ABSTRACT: Hepatitis B virus (HBV) surface antigen (HBsAg) clearance constitutes the hallmark of resolution of acute infection and is a therapeutic goal for functional cure of chronic hepatitis B. Here, we reveal the immunological landscape and mechanism of HBsAg clearance in mice. After acquiring nonopsonized HBsAg, B cells prime CD4+ T cell responses by CCR5- and EBI2-guided interaction with CD4+ T cells at follicular and interfollicular regions, respectively. Monocyte-derived macrophages transport complement-opsonized HBsAg to follicular dendritic cells (FDCs) to maintain germinal center reaction. Batf3+ XCR1+ conventional type 1 DCs (cDC1s) acquire and present HBsAg by MHC-I cross-dressing to drive CD8+ T cell responses in liver. We map the antigen-presenting cell (APC)-T cell crosstalk landscape and identify key costimulatory signals. The immune responses in patients with acute HBV infection are revealed by a single-cell transcriptome atlas. These findings revolutionize our understanding of anti-HBV immune responses and would lead to immunotherapeutic strategies for HBsAg clearance.

ORGANISM(S): Mus musculus

PROVIDER: GSE207541 | GEO | 2024/07/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The immune landscape and mechanism of hepatitis B virus surface antigen clearance [RNA-Seq]

Project description:Hepatitis B virus (HBV) surface antigen (HBsAg) clearance constitutes the hallmark of resolution of acute infection and is a therapeutic goal for functional cure of chronic hepatitis B. Here, we reveal the immunological landscape and mechanism of HBsAg clearance in mice. After acquiring nonopsonized HBsAg, B cells prime CD4+ T cell responses by CCR5- and EBI2-guided interaction with CD4+ T cells at follicular and interfollicular regions, respectively. Monocyte-derived macrophages transport complement-opsonized HBsAg to follicular dendritic cells (FDCs) to maintain germinal center reaction. Batf3+ XCR1+ conventional type 1 DCs (cDC1s) acquire and present HBsAg by MHC-I cross-dressing to drive CD8+ T cell responses in liver. We map the antigen-presenting cell (APC)-T cell crosstalk landscape and identify key costimulatory signals. The immune responses in patients with acute HBV infection are revealed by a single-cell transcriptome atlas. These findings revolutionize our understanding of anti-HBV immune responses and would lead to immunotherapeutic strategies for HBsAg clearance.

2024-07-01 | GSE207539 | GEO

Smart-seq for HBs-specific CD8+ T cells sorted from C57BL/6 mice and C57BL/6-Tg (HBV Alb-1) Bri44 HBV transgenic mice liver

Project description:Previous studies have paid more attention to hepatitis B e antigen (HBeAg) intrauterine exposure, however the effect of solely hepatitis B surface antigen (HBsAg) exposure on the immune response of offspring against hepatitis B virus (HBV) is still unclear. In this study, we investigated whether HBsAg intrauterine exposure affected the offspring's immune response against HBV and the relevant mechanism, which is important for the prevention of HBV mother-to-infant transmission.

2021-12-01 | GSE162718 | 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

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

Expression data of HBV infected liver tissue

Project description:We analyzed three clinical parameters with gene expression data from 122 liver tissues. Six healthy samples were used in validation. All hepatitis samples were HBV infected, which was validated by positive HBsAg or serum HBV-DNA. The samples with HCV infection or metabolic liver injury (e.g. fatty liver, chronic alcoholic hepatitis, etc.) were excluded. This dataset is part of the TransQST collection.

2017-02-28 | E-GEOD-83148 | biostudies-arrayexpress

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

Project description:HBsAg intrauterine exposure accelerates HBV clearance in offspring mice

| PRJNA754108 | ENA

An Hepatitis B and D Virus Infection Model Using Human Pluripotent Stem Cell-Derived Hepatocyte-Like Cells for Virus Host Interactions and Antiviral Evaluation

Project description:Current culture systems available for studying hepatitis D virus (HDV) are suboptimal. In this study, we demonstrate that hepatocyte-like cells (HLCs) derived from human pluripotent stem cells (hPSCs) are fully permissive to HDV infection across various tested genotypes. When co- infected with the helper hepatitis B virus (HBV) or transduced to express the HBV envelope protein HBsAg, HLCs effectively release infectious progeny virions. We also show that HLCs expressing HBsAg support extracellular spread of HDV, thus providing a valuable platform for testing available anti-HDV regimens. By challenging the cells along the differentiation with HDV infection, we have identified CD63 as a potential HDV/HBV co-entry factor, which was rate-limiting HDV infection in immature hepatocytes. Given their renewable source and the potential to derive hPSCs from individual patients, we propose HLCs as a promising model for investigating HDV biology. Our findings offer new insights into HDV infection and expand the repertoire of research tools available for the development of therapeutic interventions.

2024-07-29 | GSE270625 | GEO

Proteogenomic Landscape of Occult HBV Infection and HBsAg-positive HBV Infection

Project description:The pathological and physiological characteristics between HBsAg-positive HBV infection and occult hepatitis B infection (OBI) are currently unclear. This study aimed to explore the immune microenvironment in the peripheral circulation of OBI patients through proteomic sequencing, and to identify molecular biomarkers for clinical diagnosis of HBsAg-positive HBV and OBI. This research involved collection of plasma from 20 patients with OBI (negative for HBsAg but positive for HBV DNA, with HBV DNA levels < 200 IU/mL), 20 patients with HBsAg-positive HBV infection, and 10 healthy individuals. Mass spectrometry-based detection was used to analyze the proteome.

2024-08-04 | PXD054566 | iProX

Comprehensive immune profile changes to human interferon stimulation in normal and HBV-infected conditions in a humanized mouse I

Project description:The underlying mechanism of chronic hepatitis B virus (HBV) functional cure by interferon (IFN), especially in patients with low HBsAg or/and young ages, is still unresolved for lacking surrogate models. Here, we generated a type I interferon receptor humanized mouse (huIFNAR mouse) through a CRISPR/Cas9-based knock-in strategy. Then, we demonstrated that human IFN stimulated a similar gene expression profile of huIFNAR peripheral blood mononuclear cells (PBMC) to what in human PBMCs, supporting the representativeness of the novel mouse model in functionally analyzing human IFN in vivo. Next, we revealed a markedly tissue-specific gene expression atlas against human IFN treatment in the multiple organs less appreciated in healthy humans in vivo. Finally, using the AAV-HBV model, we test the antiviral effects of human interferon in this mouse. Fifteen-week human PEG-IFNα2 treatment significantly reduced HBsAg and HBeAg and even achieved HBsAg seroconversion. We observed that activation of intrahepatic monocytes and effector memory CD8 T cells by human interferon might be critical for HBsAg suppression. In conclusion, our novel huIFNAR mouse can authentically respond to human Interferon stimulation, providing a novel platform to study interferon function in vivo. The PEG-IFNα2 treatment successfully suppresses intrahepatic HBV replication and achieved HBsAg seroconversion in some mice.

2023-09-24 | GSE236814 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data