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Chromatin accessibility regions 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, an ATAC-seq (Assay for Transposase-Accessible Chromatin using sequencing) was undertaken.

ORGANISM(S): Mus musculus

PROVIDER: GSE163363 | GEO | 2021/10/11

REPOSITORIES: GEO

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Gene expression profiles 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, and RNA-seq was undertaken

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

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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

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.

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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.

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Themis differentially regulates T follicular helper cell differentiation during early and late stages of chronic viral Infection

Project description:TFH cells play an important role in chronic viral infection by helping B cells produce antibodies. Recent studies have identified a novel CD4+ T cell progenitor population in chronic LCMV infection that sustains the differentiation of TFH and other effector CD4+ T cells. However, the details of this differentiation process remain unclear. Here, we report an unprecedented dual role for Themis in regulating the differentiation of CD4+ T cell progenitors into TFH cells during chronic LCMV infection. Themis expression is strongly upregulated in TFH cells at early stages of infection, and as expected, Themis promotes TFH cell differentiation at this stage. However, unexpectedly, at the late stages of chronic LCMV infection, Themis-deficient CD4+ T cells favored TFH cell differentiation and helped control the virus by enhancing GC responses and antibody production, suggesting that Themis inhibits TFH cell differentiation at this stage. In the late stage we found that Themis inhibits the differentiation of CD4+ T cell progenitors into TFH cells through transcriptional regulation.

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Project description:Chronic viral infections incapacitate adaptive immune responses by 'exhausting' virus-specific T cells, inducing their deletion and reducing productive T cell memory. Viral infection rapidly induces death receptor Fas (CD95) expression by dendritic cells (DCs) making them susceptible to elimination by the immune response. Lymphocytic Choriomeningitis Virus (LCMV) Clone 13, which normally establishes a chronic infection, is rapidly cleared in C57Black/J mice with conditional deletion of Fas in DCs. The immune response to LCMV is characterized by an extended survival of virus-specific effector T cells. Moreover, transfer of Fas-negative DCs from non-infected mice to already-infected animals results in either complete clearance of the virus or a significant reduction of viral titers. Thus, DC-specific Fas expression plays a role in regulation of anti-viral responses and suggests a strategy for stimulation of T cells in chronically infected animals and humans in order to achieve the clearance of persistent viruses. We compared gene expression between splenic DCs from B6.FasKI and B6.CD11c-Cre.FasKI mice. DCs were isolated on day 5 after LCMV infection with 3 mice in each group, for a total of 6 samples. Spleens were collagenase-DNAse digested and sorted by flow to isolate DCs.

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