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Gene expression profiles in GC B cells during acute and chronic viral infection

ABSTRACT: To study how chronic viral infection disrupts B cell differentiation pathways and identify key intrinsic regulators in an endogenous polyclonal response, we used the comparative LCMV model. Wild-type mice were infected with either the acute (WE) versus chronic (Docile) strains of LCMV, GC B cells (CD19+IgDloCD95+CD38loCD138-) isolated 14 days post-infection, and RNA-seq was undertaken

ORGANISM(S): Mus musculus

PROVIDER: GSE163364 | GEO | 2021/10/11

REPOSITORIES: GEO

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Chromatin accessibility regions in GC B cells during acute and chronic viral infection

Project description:To study how chronic viral infection disrupts B cell differentiation pathways and identify key intrinsic regulators in an endogenous polyclonal response, we used the comparative LCMV model. Wild-type mice were infected with either the acute (WE) versus chronic (Docile) strains of LCMV, GC B cells (CD19+IgDloCD95+CD38loCD138-) isolated 14 days post-infection, an ATAC-seq (Assay for Transposase-Accessible Chromatin using sequencing) was undertaken.

2021-10-11 | GSE163363 | GEO

Gene expression profiles in GC B cells of wild-type and Bmi1 cKO mice during acute or chronic viral infection

Project description:To study how chronic viral infection disrupts B cell differentiation pathways and identify key intrinsic regulators in an endogenous polyclonal response, we used the comparative LCMV model. Wild-type or Bmi1 conditional know-out in B cells mice were infected with either the acute (WE) versus chronic (Docile) strains of LCMV, GC B cells (CD19+IgDloCD95+CD38loCD138-) isolated 14 days post-infection, and RNA-seq was undertaken

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BCR-Seq of Germinal Center B cells from mice infected with LCMV

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CXCR5+ Follicular Cytotoxic T cells Control Viral Infection in B Cell follicles

Project description:Lymphocytic Choriomeningitis Virus (LCMV) specific CD8+ T cells (P14) were transferred into congenic WT mice followed by LCMV(DOCILE) infection. CXCR5-expressing (CXCR5+) or CXCR5 non-expressing (CXCR5-) P14 were purified on day 8 after infection, and total mRNA were sequenced from these populations. mRNA of P14 from uninfected mice (Naive P14) was also sequenced. Examination of mRNA level in CXCR5 expressing P14 (CXCR5+P14) and non-expressing P14 (CXCR5-P14) from LCMV infected mice day 8 post infection. mRNA of P14 from uninfected mice (NaÃ¯ve P14) was also examined.

2016-07-31 | E-GEOD-76279 | biostudies-arrayexpress

CXCR5+ Follicular Cytotoxic T cells Control Viral Infection in B Cell follicles

2016-07-31 | GSE76279 | GEO

Gene expression profile at the single cell level of splenic LCMV-specific B cells in acute versus chronic LCMV infection [scRNA-seq, CITE-seq]

Project description:Chronic viral infection disrupts memory B cell development. We used single cell RNA sequencing (scRNA-seq) to analyze the diversity of antigen-specific B cells responding to acute versus chronic LCMV infection.

2024-02-17 | GSE225933 | GEO

Chromatin accessibility profile at the single cell level of splenic LCMV-specific B cells in acute versus chronic LCMV infection [scATAC-seq]

Project description:Chronic viral infection disrupts memory B cell development. We used single cell ATAC sequencing (scATAC-seq) to analyze chromatin accessibility in antigen-specific B cells responding to acute versus chronic LCMV infection.

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A necroptosis-independent function of RIPK3 promotes immune dysfunction and prevents control of chronic LCMV infection

Project description:Necroptosis is a lytic and inflammatory form of cell death that is highly constrained to mitigate detrimental collateral tissue damage and impaired immunity. These constraints make it difficult to define the relevance of necroptosis in diseases such as chronic and persistent viral infections and within individual organ systems. The role of necroptotic signalling is further complicated because proteins essential to this pathway, such as receptor interacting protein kinase 3 (RIPK3) and mixed lineage kinase domain-like (MLKL), have been implicated in roles outside of necroptotic signalling. We sought to address this issue by individually defining the role of RIPK3 and MLKL in chronic lymphocytic choriomeningitis virus (LCMV) infection. We investigated if necroptosis contributes to the death of LCMV-specific CD8+ T cells or virally infected target cells during infection. We provide evidence showing that necroptosis was redundant in the pathogenesis of acute forms of LCMV (Armstrong strain) and the early stages of chronic (Docile strain) LCMV infection in vivo. The number of immune cells, their specificity and reactivity towards viral antigens and viral loads are not altered in the absence of either MLKL or RIPK3 during acute and during the early stages of chronic LCMV infection. However, we identified that RIPK3 promotes immune dysfunction and prevents control of infection at later stages of chronic LCMV disease. This was not phenocopied by the loss of MLKL indicating that the phenotype was driven by a necroptosis-independent function of RIPK3. We provide evidence that RIPK3 signaling evoked a dysregulated type 1 interferone response which we linked to an impaired antiviral immune response and abrogated clearance of chronic LCMV infection.

2023-03-12 | GSE224066 | GEO

Changes in chromatin accessibility assocaiated with CD8 T cell responses to viral infections

Project description:The goal of this study was to identify the molecular programming using ATAC-seq of CD8 T cells responding to different viral infections. Mice were infected with either LCMV Armstrong to model an acute infection or LCMV Clone-13 to model a chronic infection. At various time points following infection, virus-specific CD8 T cells were purified and ATAC-seq performed. These data identify the changes in chromatin accessibility associated with acute infections and the establishment of functional memory versus those accessibility changes associated with chronic infection.

2017-01-31 | GSE83081 | GEO

Memory-like CD8 T-cells sustain the immune response to chronic viral infections.

Project description:We have discovered a small subpopulation of virus-specific CD8 T-cells that sustains the T-cell response in chronic infections. These cells are defined by - and depend on - the expression of the transcription factor Tcf1 (T cell factor 1) and show key characteristics of central memory cells while lacking an effector signature. Unlike conventional memory cells, Tcf1+ T-cells display hallmarks of an âexhaustedâ phenotype, including the expression of certain inhibitory receptors. Naive Tcf1-GFP+ P14 cells (Naive) were transferred into Vb5 recipient mice (CD45.1) prior to infection with LCMV clone 13 (c13). Tcf1-GFP+ P14 cells (chronic Tcf1+) and Tcf1-GFP- P14 cells (chronic Tcf1-) were flow sorted on day 28 post infection. Naive Tcf1-GFP+ P14 cells (Naive) were also transferred into C57BL/6 hosts (CD45.1.2) prior to infection with LCMV Armstrong (Arm). Tcf1-GFP+ P14 cells (memory Tcf1+) and Tcf1-GFP- P14 cells (memory Tcf1-) were flow sorted on day 28 post infection. Total RNA was extracted, cDNA libraries prepared and sequencing was performed using Illumina HiSeq 2500 technology.

2016-08-22 | E-GEOD-83978 | biostudies-arrayexpress

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