IFNAR1 Signaling in NK Cells Promotes Persistent Virus Infection
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA613837 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11363335.fastq.gz | Fastqsanger.gz | |||
| SRR11363336.fastq.gz | Fastqsanger.gz | |||
| SRR11363337.fastq.gz | Fastqsanger.gz | |||
| SRR11363338.fastq.gz | Fastqsanger.gz | |||
| SRR11363339.fastq.gz | Fastqsanger.gz |
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Project description:Inhibition of IFN-I signaling promotes the control of persistent virus infection, but the underlying mechanisms remain poorly understood. Here we report that genetic ablation of IFNAR1 specifically in NK cells led to elevated numbers of T follicular helper cells, germinal center B cells, and plasma cells, resulting in hastened virus clearance comparable to IFNAR1 blockade by an IFNAR1 neutralizing antibody. Antigen-specific B cells and antiviral antibodies were essential for the accelerated control of LCMV Cl13 infection following IFNAR1 blockade. IFNAR1 signaling in NK cells promoted NK cell maturation, function, and killing of antigenspecific CD4 and CD8 T cells. Therefore, Inhibition of IFN I signaling in NK cells enhances CD4 and CD8 T cell responses, elevates humoral immune response, and thereby facilitates the control of persistent virus infection.
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Project description:Inhibition of type 1 interferon (IFN-I) signaling promotes the control of persistent virus infection, but the underlying mechanisms remain poorly understood. Here, we report that genetic ablation of Ifnar1 specifically in natural killer (NK) cells led to elevated numbers of T follicular helper cells, germinal center B cells, and plasma cells and improved antiviral T cell function, resulting in hastened virus clearance that was comparable to IFNAR1 neutralizing antibody treatment. Antigen-specific B cells and antiviral antibodies were essential for the accelerated control of LCMV Cl13 infection following IFNAR1 blockade. IFNAR1 signaling in NK cells promoted NK cell function and general killing of antigen-specific CD4 and CD8 T cells. Therefore, inhibition of IFN-I signaling in NK cells enhances CD4 and CD8 T cell responses, promotes humoral immune responses, and thereby facilitates the control of persistent virus infection.
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Project description:To understand the effect of type-I IFN signaling directly on CD8+ T cells following an LCMV infection we compared the overall gene expression of WT and Ifnar1-/- T cells following an LCMV infection. WT and Ifnar1-/- P14 cells were sorted from infected mice (day 3) that were depleted of NK cells or left untreated. Each sample and condition (WT or IFNAR) was performed in triplicates
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Project description:Epigenetic changes, including histone methylation, control T cell differentiation and memory formation, though the enzymes that mediate these processes are not clear. We show that UTX, a histone H3 lysine 27 (H3K27) demethylase, promotes the generation of T follicular helper (Tfh) cells, a CD4+ T cell subset essential for B cell antibody generation and clearance of chronic viral infections. Mice with T cell specific UTX deletion (UTX TKO mice) had fewer Tfh cells, showed defective germinal center formation, lacked virus-specific IgG production, and were unable to resolve chronic lymphocytic choriomeningitis virus infection. In UTX TKO T cells, decreased expression of IL-6R±, and other Tfh-related loci, was associated with increased H3K27 methylation. Additionally, Turner Syndrome subjects, who are predisposed to chronic ear infections, have reduced UTX expression in immune cells and decreased Tfh frequency. Thus, we identify a critical link between UTX in T cells and immunity to infection. Mice were infected with chronic LCMV and sorted for Tfh on day 21 pi (sorted for: CD4+CXCR5+CD62Llo T cell). ChIP-Seq and RNA-Seq on WT and Utx KO cells.
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Project description:The experimental data indicate that during a persistent infection, lymphocytic choriomeningitis virus (LCMV) may both directly or indirectly modulate the regulatory cellular processes and alter the cellular functions that are not critical for the survival, but are needed for the homeostasis in the organism. Two-dimensional differential in-gel electrophoresis (2D-DIGE) and MALDI-TOF MS/MS analyses were used to determine the cellular proteome response of HeLa cell line to persistent LCMV infection. Quantitative analysis revealed 24 differentially abundant proteins, half of which were up-regulated and the rest down-regulated. Functional categorization showed that LCMV-responsive proteins were mainly involved in metabolism, stress and defense responses. Among identified proteins, significant changes were found for peroxiredoxins, family of antioxidant enzymes. Decreased amount of these antioxidant proteins was accompanied with the elevation of ROS content in infected cells.
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Project description:Epigenetic changes, including histone methylation, control T cell differentiation and memory formation, though the enzymes that mediate these processes are not clear. We show that UTX, a histone H3 lysine 27 (H3K27) demethylase, promotes the generation of T follicular helper (Tfh) cells, a CD4+ T cell subset essential for B cell antibody generation and clearance of chronic viral infections. Mice with T cell specific UTX deletion (UTX TKO mice) had fewer Tfh cells, showed defective germinal center formation, lacked virus-specific IgG production, and were unable to resolve chronic lymphocytic choriomeningitis virus infection. In UTX TKO T cells, decreased expression of IL-6R±, and other Tfh-related loci, was associated with increased H3K27 methylation. Additionally, Turner Syndrome subjects, who are predisposed to chronic ear infections, have reduced UTX expression in immune cells and decreased Tfh frequency. Thus, we identify a critical link between UTX in T cells and immunity to infection.
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Project description:In this study, we show that CD27+ memory like NK cells generated following Zika virus infection exhibited stem-like features viz., self-renewal pathway, differentiation into effector cells and longer telomeres, and greater therapeutic potential than CD27- and naive CD27+ NK cells when adoptively transferred to Zika virus infected mice. In addition, epigenetic landscape of CD27+ memory like NK is markedly different compared to CD27- NK cells.
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Project description:is involved in the formation of immune signaling complexes. To date only limited and moreover 35 conflicting data exist regarding the role of ADAP in NK cells. To extend existing knowledge we 36 investigated ADAP-dependency of NK cells in the context of in vivo infection with the intracellular 37 pathogen Listeria monocytogenes (Lm). Ex vivo analysis of infection-primed NK cells revealed 38 impaired expression of IFN-γ and chemokines as well as impaired cytotoxic capacity in NK cells 39 lacking ADAP as indicated by reduced CD107a surface expression and inefficient perforin 40 production. However, ADAP-deficiency had no global effect on NK cell morphology or intracellular 41 distribution of CD107a-containing vesicles. Proteomic definition of ADAPko and wild type NK cells 42 did not uncover obvious differences in protein composition during the steady state and moreover, 43 similar early response patterns were induced in NK cells upon infection independent of the genotype. 44 In line with protein network analyses that suggested an altered migration phenotype in naïve 45 ADAPko NK cells, in vitro migration assays uncovered significantly reduced migration of both naïve 46 as well as infection-primed ADAPko NK cells compared to wild type NK cells. We propose that this 47 migration defect might account at least in part for the fact that during in vivo infection significantly 48 lower numbers of ADAPko NK cells accumulate in the spleen i.e. the site of infection. In conclusion, 49 we show here that during systemic Lm infection in mice ADAP is essential for efficient cytokine and 50 chemokine production, cytotoxic capacity and migration of NK cells.
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