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Memory-like HCV-specific CD8+ T cells retain a molecular scar after cure of chronic HCV infection

ABSTRACT: Memory-like HCV-specific CD8+ T cells retain a molecular scar after cure of chronic HCV infection

PROVIDER: PRJNA631795 | ENA |

REPOSITORIES: ENA

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Memory-like HCV-specific CD8+ T cells retain a chronic scar after cure of chronic HCV infection

Project description:Memory-like HCV-specific CD8+ T cells retain a chronic scar after cure of chronic HCV infection

| PRJNA631746 | ENA

Memory-like HCV-specific CD8+ T cells retain a molecular scar after cure of chronic HCV infection

Project description:Investigation of phenotypical changes between exhausted HCV-specific CD8+ T cells during chronic infection and after DAA-mediated cure investigation of heterogeneity withhin the HCV-specific CD8+ T cell population

2020-09-07 | GSE150345 | GEO

Memory-like HCV-specific CD8+ T cells retain a chronic scar after cure of chronic HCV infection

2020-09-08 | GSE150305 | GEO

Memory-like HCV-specific CD8+ T cells retain a chronic scar after cure of chronic HCV infection

Project description:Chronic hepatitis C virus (HCV) infection is associated with CD8+ T-cell exhaustion characterized by limited effector functions and thus compromised anti-viral activity. Exhausted HCV-specific CD8+ T cells are comprised of memory-like and terminally exhausted CD8+ T-cell subsets. So far, little is not known about the molecular profile and fate of these cells after elimination of chronic antigen stimulation by direct acting antiviral therapy (DAA). Here, we report an antigen-driven molecular core signature underlying exhausted CD8+ T-cell subset heterogeneity in chronic viral infection with a progenitor/progeny relationship of memory-like and terminally exhausted HCV-specific CD8+ T cells via an intermediate stage. Furthermore, transcriptional profiling reveals that the memory-like cells remain after DAA-mediated cure while terminally exhausted HCV-specific CD8+ T-cell subsets are lost. Thus, the memory polarization of the overall HCV-specific CD8+ T-cell response after cure does not result from re-differentiation of exhausted T cells. Consequently, antigen elimination has little impact on the exhausted core signature of memory-like CD8+ T cells that remains clearly different from bona fide T-cell memory. These results identify a molecular signature of T-cell exhaustion that is imprinted like a chronic scar in HCV-specific CD8+ T cells even after HCV cure, highlighting the requirement of re-programming to elicit full effector potential of exhausted T cells.

| EGAS00001004538 | EGA

Endothelial Cells retain inflammatory memory through chromatin remodeling

Project description:Endothelial Cells retain inflammatory memory through chromatin remodeling

| PRJNA1271511 | ENA

Endothelial Cells retain inflammatory memory through chromatin remodeling [ATAC]

Project description:Endothelial Cells retain inflammatory memory through chromatin remodeling [ATAC]

| PRJNA1287566 | ENA

Endothelial Cells retain inflammatory memory through chromatin remodeling II

Project description:Endothelial Cells retain inflammatory memory through chromatin remodeling II

| PRJNA1273182 | ENA

Antiviral HCV Treatment Induces Rapid Proteomic and Phospho-proteomic Changes in Hepatic Interferon and ERK1/2 Signaling Pathways

Project description:Although treatment of chronic hepatitis C virus (HCV) infection with direct acting antivirals (DAAs) results in high rates of cure, liver fibrosis does not resolve immediately after HCV eradication. Resolution of fibrosis occurs in some, but not all patients, after HCV cure, and hepatic decompensation and hepatocellular carcinoma can still occur in patients with pre-existing cirrhosis. We hypothesized that evaluation of the host liver proteome in the context of HCV treatment would provide insight into how inflammatory and fibrinogenic pathways change upon HCV eradication. We evaluated the whole liver proteome and phosphoproteome using paired liver biopsies from 8 HCV-infected patients collected before or immediately after treatment with DAAs in clinical trials. We identify interferon stimulated proteins as the predominant pathways that decrease with HCV treatment, which is consistent with previous analyses of the liver transcriptome during DAA therapy. While there was no change in the proteome of pathways associated with liver fibrosis, we identified a decrease in the phosphoproteome signature for ERK1/ERK2 as a result of HCV treatment. Conclusion: There is a reduction in the endogenous interferon-mediated antiviral response and alterations in the phosphoproteome that may precede resolution of fibrosis in the liver immediately after treatment of HCV with DAAs.

2023-03-11 | PXD024846 | Pride

Pathogenic IgE-fated memory B cell responses retain functional plasticity

Project description:Pathogenic IgE-fated memory B cell responses retain functional plasticity

| PRJEB102286 | ENA

Endothelial Cells retain inflammatory memory through chromatin remodeling [ATAC-seq]

Project description:Endothelial Cells retain inflammatory memory through chromatin remodeling [ATAC-seq]

| PRJNA1271585 | ENA