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Gene expression profiles of CD4+CD25+ regulatory T cells during acute and chronic viral infection

ABSTRACT: Regulatory T (Treg) cells act as terminators in the case of T cell immunity during the acute phase of viral infection. However, their roles in chronic viral infection are not completely understood. We compared the phenotype and function of Treg cells during acute and chronic viral infection using lymphocytic choriomeningitis virus-infected mouse models. Chronic infection, unlike acute infection, led to induction of Treg cells and upregulation of various inhibitory receptors. Treg cells isolated from chronically infected mice (chronic Treg cells) displayed greater suppressive capacity for inhibiting T cell proliferation and subsequent cytokine production than those from naïve (naive Treg cells) or acutely infected mice (acute Treg cells). These gene expression profiles provided evidence that chronic Treg cells display characteristics distinct from either naive or acute Treg cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE63876 | GEO | 2014/12/05

SECONDARY ACCESSION(S): PRJNA269307

REPOSITORIES: GEO

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Gene expression profiles of CD4+CD25+ regulatory T cells during acute and chronic viral infection

Project description:Regulatory T (Treg) cells act as terminators in the case of T cell immunity during the acute phase of viral infection. However, their roles in chronic viral infection are not completely understood. We compared the phenotype and function of Treg cells during acute and chronic viral infection using lymphocytic choriomeningitis virus-infected mouse models. Chronic infection, unlike acute infection, led to induction of Treg cells and upregulation of various inhibitory receptors. Treg cells isolated from chronically infected mice (chronic Treg cells) displayed greater suppressive capacity for inhibiting T cell proliferation and subsequent cytokine production than those from naM-CM-/ve (naive Treg cells) or acutely infected mice (acute Treg cells). These gene expression profiles provided evidence that chronic Treg cells display characteristics distinct from either naive or acute Treg cells. Mouse splenic CD4+CD25+ regulatory T cells were analyzed at 0 day and 16 day after acute or chronic viral infection with LCMV Arm or CL13, respectively.

2014-12-05 | E-GEOD-63876 | biostudies-arrayexpress

Chronic viral infection of naive, effector, memory and exhausted virus-specific CD8 T cells

Project description:CD8 T cells normally differentiate from resting naïve T cells into function effector and then memory CD8 T cells following acute infections. During chronic viral infections, however, virus-specific CD8 T cells often become exhausted. We used microarrays to examine the gene expression differences between naive, effector, memory and exhausted virus-specific CD8 T cells following lymphocytic choriomeningitis virus infection. Keywords: infection response

2007-11-27 | GSE9650 | GEO

Transcription profiling of mouse naive, effector, memory and exhausted virus-specific CD8 T cells after chronic viral infection

Project description:CD8 T cells normally differentiate from resting naÃ¯ve T cells into function effector and then memory CD8 T cells following acute infections. During chronic viral infections, however, virus-specific CD8 T cells often become exhausted. We used microarrays to examine the gene expression differences between naive, effector, memory and exhausted virus-specific CD8 T cells following lymphocytic choriomeningitis virus infection. Experiment Overall Design: Three or four independent samples were sorted by flow cytometry for each cell type (naive, effector, memory and exhausted) virus-specific CD8 T cells. RNA was extracted and hybridized to Affymetrix microarrays.

2008-06-16 | E-GEOD-9650 | biostudies-arrayexpress

Antibody repertoire sequencing of blood and bone marrow plasma cell compartments following lymphocytic choriomeningitis virus infection

Project description:Antibody repertoire sequencing of blood and bone marrow plasma cell compartments following lymphocytic choriomeningitis virus infection. Heavy chain repertoires of 5 uninfected mice, 5 acutely infected mice and 5 chronically infected mice were longitudinally sequenced over 80 days. All samples are named according to the following scheme: dpi#_cohort$_R&.fastq.gz . dpi = days post infection = for all samples following the start of infection. Those samples starting with dm10 correspond to blood samples taken before the introduction of any virus. # = time point post virus infection cohort=acute (LCMV), chronic (LCMV), or naive (uninfected) animals $= mouse number, 1-5 R&=paired read, either R1 or R2 Those samples with \"bmpc\" in title correspond to sorted plasma cells (CD138hi, CD19lo) from bone marrow Example: dpi70_chronic3_R2.fastq.gz == blood repertoire 70 days post chronic LCMV infection in chronically-infected mouse#3

2020-01-16 | E-MTAB-8585 | biostudies-arrayexpress

Type I interferon signaling attenuates Regulatory T cells function in LCMV infection

Project description:Regulatory T cells (Tregs) play a cardinal role in the immune system by suppressing detrimental autoimmune responses, but their role in acute and chronic infectious diseases remains unclear. We recently demonstrated that IFN- receptor (IFNAR) signaling promotes Treg function in autoimmunity. To dissect the functional role of IFNAR-signaling in Tregs during acute and chronic viral infection, we infected Treg-specific IFNAR deficient (IFNARfl/flxFoxp3YFP-Cre) mice with LCMV Armstrong and Clone-13. In both models, IFNARfl/flxFoxp3YFP-Cre mice Tregs expressed enhanced expression of Treg associated activation antigens. The enhanced activated phenotype was also seen when we compared the transcriptomes of IFNARfl/flxFoxp3YFP-Cre and wild type (WT) Tregs by RNA-Seq on day 25-post Clone-13 infection. LCMV-specific CD8+ T cells from IFNARfl/flxFoxp3YFP-Cre mice produced less antiviral IFN and TNF in both acute and chronic LCMV. In the chronic model, the numbers of anti-viral effector and memory CD8+ T cells were decreased in IFNARfl/flxFoxp3YFP-Cre mice and the effector CD4+ and CD8+ T cells exhibited a phenotype compatible with enhanced exhaustion. IFNARfl/flxFoxp3YFP-Cre mice cleared Armstrong infection normally, but had higher viral titers in sera, kidneys and lungs than WT mice during chronic infection. Thus, type I IFN signaling in Tregs is context-dependent, resulting in enhanced suppressor function in some models of autoimmunity, but decreased suppressor function in acute and chronic viral infection.

2017-10-24 | GSE93909 | GEO

Bulk RNA seq of intestinal immune cells from naïve, LCMV-Arm and LCMV-Cl13 infected mice

Project description:We report that the gastrointestinal tract (GIT) is a previously unappreciated long-term reservoir of chronic LCMV-Cl13 infection, and, chronic viral replication in the GIT has a profound effect on the local immune compartment as well as the development of subsequent immune responses. CD45+ immune cells were sorted and analyzed by RNAseq from the small and large intestines of naive mice, or mice infected 30 days prior with LCMV-Arm (acute virus) or LCMV-Cl13 (chronic virus). We show that GIT immune cells from acute and chronically infected mice differ substantially from naive mice; chronically infected mice show increases in genetic pathways involved in T cell activation and killing, inflammasome activation and interferon signaling; chronically infected mice show reduced expression of genes involved in T cell memory and antigen presenting cell activation; and chronic infection induces metabolic changes unique to the small but not large intestinal immune compartment.

2020-08-11 | GSE142303 | GEO

PRONOUNCED PHENOTYPE IN ACTIVATED TREG CELLS DURING A CHRONIC HELMINTH INFECTION

Project description:Although several markers have been associated with the characterization of regulatory T cells (Treg) and their function, no studies have investigated the dynamics of their phenotype during infection. Since the necessity of Treg to control immunopathology has been demonstrated, we used the chronic helminth infection model S. mansoni to address the impact on the Treg gene repertoire. Before gene expression profiling we first chose to study the localization and antigen-specific suppressive nature of classically defined Treg during infection. Presence of Foxp3+ cells were found especially in the periphery of granulomas and isolated CD4+CD25hiFoxp3+ Treg from infected mice blocked IFN-gamma and IL-10 cytokine secretion from infected CD4+CD25- effector T cells (Teff). Furthermore the gene expression patterns of Treg and Teff showed that in total 474 genes were significantly regulated during chronic schistosomiasis. Upon k-means clustering we identified genes exclusively regulated in all four populations including Foxp3, CD103, GITR, OX40 and CTLA-4: classical Treg markers. During infection however, several non-classical genes were up-regulated solely within the Treg population such as Slpi, Gzmb, Mt1, Fabp5, Nfil3, Socs2, Gpr177 and Klrg1. Using RT-PCR we confirmed aspects of the microarray data and in addition showed that the expression profile of Treg from S. mansoni-infected mice is simultaneously unique and comparative with Treg derived from other infections Regulatory T cells (Treg) or effector T cells (Teff) were FACS-sorted as CD4+CD25+ or CD4+CD25- from mesenteric lymph nodes (MLN) of naive mice or from mice infected with Schistosoma mansoni. Affymetrix MOE430A 2.0 genechips were used to identify genes differentially expressed in Treg or Teff under resting or infected conditions.

2010-04-12 | E-GEOD-17580 | biostudies-arrayexpress

Loss of Fas (CD95) expression by dendritic cells protects from a chronic viral infection

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.

2014-05-09 | E-GEOD-57443 | biostudies-arrayexpress

Loss of Fas (CD95) expression by dendritic cells protects from a chronic viral infection

2014-05-09 | GSE57443 | GEO

Comparison of Trail+/+ versus Trail-/- splenic NK cells from naïve and LCMV-infected mice

Project description:Investigation of the change of the Trail-dependent NK cell transcriptome during short-term (24h) infection with lymphocytic choriomeningitis virus (LCMV). RNA sequencing-based transcriptomics analysis was performed in spleen-isolated (NK1.1+CD3-) NK cells from 3 naïve Trail+/+ mice, 3 naive Trail-/- mice, 4 LCMV-infected Trail+/+ mice, and 4 LCMV-infected Trail-/- mice.

2019-08-27 | E-MTAB-7562 | biostudies-arrayexpress

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