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IL-1B signaling in dendritic cells induces antiviral interferon responses

ABSTRACT: IL-1B signaling in dendritic cells induces antiviral interferon responses

PROVIDER: PRJNA429565 | ENA |

REPOSITORIES: ENA

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IL-1B signaling in dendritic cells induces antiviral interferon responses

Project description:Activation of interferon-stimulated gene (ISG) responses is critical for control of viral infection. We recently identified that stimulation of the NLRP3 inflammasome and mobilization of the inflammatory cytokine IL-1β act as critical host restrictive pathways against West Nile virus (WNV) in a mechanism dependent on the regulation of ISGs. In order to define the mechanism by which IL-1β regulates these antiviral immune programs, we utilized global transcriptome analysis in myeloid cells, known targets of WNV replication to define gene signatures required for IL-1β driven antiviral responses. Surprisingly, we found IL-1β dependent activation of interferon-beta (IFN-β) and ISGs at late times following IL-1β treatment. Expression of these antiviral innate immune genes was found to be dependent on activation of IRF3 and appears to reflect a general shift in IL-1β signaling from an inflammatory response early following treatment to an anti-inflammatory type-I IFN mediated response at later times post-treatment. These data demonstrate that inflammatory and antiviral signals integrate to control viral infection. Strategies to co-opt these cytokine activated antiviral signatures can act as novel targeted therapeutic strategies tailored specifically to individual pathogens.

2018-01-12 | GSE109069 | GEO

Type I Interferon promotes MxA-dependent IL-1b release in SLE monocytes

Project description:Systemic lupus erythematosus (SLE) is characterized by upregulation of Type Ι Interferon (IFN) and widespread inflammation. However, blocking the IFN pathway benefits a fraction of patients, pointing to additional pathogenic players. Here we describe monocytes (Mo) undergoing erythrophagocytosis and co-expressing IFN-inducible genes (ISGs) and interleukin-1b (IL-1b) in patients with active disease. This phenotype is recapitulated in vitro upon internalization of red blood cells carrying mitochondria (Mito+ RBCs), a feature of SLE. While ISG expression requires the interaction between Mito+ RBC-derived mitochondrial DNA (mtDNA) and cGAS, the production of IL-1b entails Mito+ RBC-derived mitochondrial RNA (mtRNA) triggering RIG-I-like receptor (RLR) activation. This leads to the cytosolic release of Mo-derived mtDNA and activation of the NLRP3 inflammasome. Importantly, the Type I IFN-inducible protein myxovirus resistant protein 1 (MxA) enables IL-1b release by routing this cytokine into a trans-Golgi network (TGN)-mediated unconventional secretory pathway. As Type I IFN and IL-1b are thought to counter-regulate each other, our study highlights an unprecedented synergy between these two cytokine pathways in SLE.

2024-10-07 | GSE211361 | GEO

Tonic type I interferon signaling optimizes the antiviral function of plasmacytoid dendritic cells

Project description:Tonic type I interferon signaling optimizes the antiviral function of plasmacytoid dendritic cells

| PRJNA1058485 | ENA

Tonic type I interferon signaling optimizes the antiviral function of plasmacytoid dendritic cells [Multiome]

Project description:Tonic type I interferon signaling optimizes the antiviral function of plasmacytoid dendritic cells [Multiome]

| PRJNA1058464 | ENA

Tonic type I interferon signaling optimizes the antiviral function of plasmacytoid dendritic cells [CITE-seq]

Project description:Tonic type I interferon signaling optimizes the antiviral function of plasmacytoid dendritic cells [CITE-seq]

| PRJNA1058488 | ENA

Modified Stat1 Confers Enhanced Interferon Responsiveness and Improved Baseline Antiviral Host Defense

Project description:U3A cells stably expressing wild-type STAT1 or STAT1-CC were treated with interferon beta (10U/ml) or control for 24 hours to assess effects of stat1 modifications, interferon, and the interaction on gene expression. Keywords: interferon, STAT1, STAT1-CC, STAT1CC, STAT-1C, antiviral RNA was isolated from stable U3A-STAT1 lines stably expressing wild-type STAT1 or STAT1CC, after 24 hour treatment with interferon beta (10U/ml) or control.

2015-09-01 | E-GEOD-61413 | biostudies-arrayexpress

Type I Interferon promotes MxA-dependent IL-1b release in SLE monocytes

Project description:Type I Interferon promotes MxA-dependent IL-1b release in SLE monocytes

| PRJNA869965 | ENA

Tonic type I interferon signaling optimizes the antiviral function of plasmacytoid dendritic cells [Bulk RNA-seq]

Project description:Tonic type I interferon signaling optimizes the antiviral function of plasmacytoid dendritic cells [Bulk RNA-seq]

| PRJNA1058465 | ENA

A cryptic sensor for HIV-1 activates antiviral innate immunity in dendritic cells

Project description:Dendritic cells (DC) serve a key function in host defense, linking innate detection of microbes to the activation of pathogen-specific adaptive immune responses. Whether there is cell-intrinsic recognition of HIV-1 by host innate pattern-recognition receptors and subsequent coupling to antiviral T cell responses is not yet known. DC are largely resistant to infection with HIV-1, but facilitate infection of co-cultured T-helper cells through a process of trans-enhancement. We show here that, when DC resistance to infection is circumvented, HIV-1 induces DC maturation, an antiviral type I interferon response and activation of T cells. This innate response is dependent on the interaction of newly-synthesized HIV-1 capsid (CA) with cellular cyclophilin A (CypA) and the subsequent activation of the transcription factor IRF3. Because the peptidyl-prolyl isomerase CypA also interacts with CA to promote HIV-1 infectivity, our results suggest that CA conformation has evolved under opposing selective pressures for infectivity versus furtiveness. Thus, a cell intrinsic sensor for HIV-1 exists in DC and mediates an antiviral immune response, but it is not typically engaged due to absence of DC infection. The virulence of HIV-1 may be related to evasion of this response, whose manipulation may be necessary to generate an effective HIV-1 vaccine. We analyzed the gene expression profiles of uninfected human monocyte-derived dendritic cells (MDDCs) and MDDCs infected with an envelope-defective GFP-encoding VSV-G-pseudotyped HIV-1 vector (HIVGFP(G)) and with VSV-G pseudotyped virus-like particles derived from SIVmac to deliver Vpx (SIVVLP(G)), alone or in combination. Cells were infected at day 4 of differentiation and cells were harvested 48 hours later. RNA was extracted with TRIzol. RNA was labeled and hybridized to Human Genome U133A 2.0 arrays arrays following the Affymetrix protocols. Data were analyzed in R and Bioconductor.

2010-09-09 | E-GEOD-22589 | biostudies-arrayexpress

Tonic type I interferon signaling optimizes the antiviral function of plasmacytoid dendritic cells [Multiome]

Project description:Plasmacytoid dendritic cells (pDCs) mount powerful type I interferon (IFN-I) responses against viruses and virus-derived nucleic acids. Only a small fraction of pDCs produces high levels of IFN-I, yet neither the molecular basis nor the purpose of this functional heterogeneity are known. We report that naive murine pDCs comprise three transcriptionally (but not epigenetically) distinct subsets. This heterogeneity is generated by tonic IFN-I signaling elicited in part by the cGAS/STING and TLR9 pathways. A small "IFN-I-naive" subset (pDC-A) was expanded in STING deficiency or after transient IFN-I receptor blockade, but was abolished by exogenous IFN-I. pDC-A showed strong cytokine responses yet were susceptible to infection with vesicular stomatitis virus (VSV). Conversely, the majority of pDCs comprised the "IFN-I-primed" subsets (pDC-B/C) that showed lower IFN-I responses but were resistant to VSV. Thus, tonic IFN-I signaling decreases the cytokine-producing capacity of pDCs but increases their virus resistance, achieving the optimal functional balance for antiviral responses.

2025-08-05 | GSE252189 | GEO

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