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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

Project description:To study how acute or chronic viral infection (LCMV-WE or Docile) affect somatic hypermutation and/or affinity maturation of Germinal Center B cells, wild-type or Bmi1-deleted mice were infected with either the acute (WE) versus chronic (Docile) strains of LCMV, GC B cells (CD19+IgDloCD95+CD38loCD138-) were isolated 14 days post-infection and thei BCR was sequenced.

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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

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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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Expression Data from in vivo Tfh vs GC Tfh vs non-Tfh

Project description:CD4 T cell help is critical for both the generation and maintenance of germinal centers, and T follicular helper (TFH) cells are the CD4 T cell subset required for this process. SAP (SH2D1A) expression in CD4 T cells is essential for germinal center development. However, SAP-deficient mice have only a moderate defect in TFH differentiation as defined by common TFH surface markers. CXCR5+ TFH cells are found within the germinal center as well as along the boundary regions of T/B cell zones. Here we show that germinal center associated T cells (GC TFH) can be identified by their co-expression of CXCR5 and the GL7 epitope, allowing for phenotypic and functional analysis of TFH and GC TFH populations. Here we show GC TFH are a functionally discrete subset of further polarized TFH cells, with enhanced B cell help capacity and a specialized ability to produce IL-4 in a TH2-independent manner. Strikingly, SAP-deficient mice have an absence of the GC TFH subset and SAP- TFH are defective in IL-4 and IL-21 production. We further demonstrate that SLAM (Slamf1, CD150), a surface receptor that utilizes SAP signaling, is specifically required for IL-4 production by GC TFH. GC TFH cells require IL-4 and IL-21 production for optimal help to B cells. These data illustrate complexities of SAP-dependent SLAM family receptor signaling, revealing a prominent role for SLAM receptor ligation in IL-4 production by germinal center CD4 T cells but not in TFH and GC TFH differentiation. Analysis of in vivo polyclonal GC Tfh vs Tfh vs Non-Tfh eight days after LCMV viral infection. Analysis of in vivo follicular helper CD4 T cells (CXCR5high GL7low), versus germinal center follicular helper CD4 T cells (CXCR5hi GL7hi), versus non-follicular helper CD4 T cells (CXCR5low) eight days after viral infection.

2010-04-28 | E-GEOD-21380 | biostudies-arrayexpress

Transcriptional profile of B cell susbets

Project description:Inflammatory (B220+ CD19+ CD44+ CD11c+ Tbet-AmCyanhi), GC (B220+ IgDlo CD95+ GL-7+), and naive follicular B cells (B220+ CD19+ IgDhi CD23+) were sorted from male Tbet-AmCyan reporter mice at day 12 post infection with LCMV-Armstrong. RNA-seq was employed to compare the transcriptomes of these three B cell populations.

2022-01-19 | GSE150124 | 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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Transcription profiling of mouseWT vs CD137L-/- GC B cells

Project description:WT and CD137L-/- mice of 8-12 weeks old were immunized intra-peritoneally with 50 Âµg chicken gamma- globulin conjugated to 4-hydroxy-3-nitrophenylacetyl (NP-CG) in alum or infected intranasally with 25 hemagglutinin units of influenza virus strain A/NT/60/68 in 50 Âµl HBSS. Nine days after immunization or infection, B cells were enriched from pooled spleens and lymph nodes of 4 mice per test group by means of magnetic labelled bead cell separation (MACS) using anti-mouse BD ImagTM CD45R/B220-particles DM. The B220+ MACS-sorted populations were stained with anti-GL7-FITC and anti-CD19-PE to sort CD19+GL7+ GC and CD19+GL7- non-GC B lymphocytes by flow cytometry on a FACSAria (BD). Around 1 million cells of each sample were obtained. These cells were spun down and the pellet was frozen in liquid nitrogen and kept at -80 ÂºC before RNA extraction.

2009-07-24 | E-NCMF-29 | biostudies-arrayexpress

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