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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE252191 | GEO | 2025/08/05

REPOSITORIES: GEO

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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

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

2025-08-05 | GSE252190 | GEO

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

2025-08-05 | GSE252188 | 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

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

Human plasmacytoid dendritic cell accumulation amplifies their type 1 interferon production.

Project description:To determine the potential consequences of plasmacytoid dendritic cell (pDC) accumulation in tissue sites observed in several autoimmune diseases, we measured type 1 interferon production from circulating human pDCs as a function of pDC concentration. The effects of interferon-alpha and blockade of the type 1 interferon receptor (IFNAR) on human pDC type 1 interferon and interferon-inducible transcription and protein production were measured. Human pDCs became far more efficient producers of interferon-alpha at concentrations beyond those normally present in blood, through an IFNAR-dependent mechanism. Extracellular interferon-alpha increased pDC production of type 1 interferons. The accumulation of pDCs in diseased tissue sites allows marked non-linear amplification of type 1 interferon production locally. The role of the IFNAR-dependent mechanism of interferon production by human pDCs is greater than previously suggested. IFNAR blockade has potential for diminishing type 1 interferon production by all human cells.

| S-EPMC2892243 | biostudies-literature

Plasmacytoid dendritic cell ablation impacts early interferon responses and antiviral NK and CD8(+) T cell accrual.

Project description:Plasmacytoid dendritic cells (pDCs) mediate type I interferon (IFN-I) responses to viruses that are recognized through the Toll-like receptor 7 (TLR7) or TLR9 signaling pathway. However, it is unclear how pDCs regulate the antiviral responses via innate and adaptive immune cells. We generated diphtheria toxin receptor transgenic mice to selectively deplete pDCs by administration of diphtheria toxin. pDC-depleted mice were challenged with viruses known to activate pDCs. In murine cytomegalovirus (MCMV) infection, pDC depletion reduced early IFN-I production and augmented viral burden facilitating the expansion of natural killer (NK) cells expressing the MCMV-specific receptor Ly49H. During vesicular stomatitis virus (VSV) infection, pDC depletion enhanced early viral replication and impaired the survival and accumulation of virus-specific cytotoxic T lymphocytes. We conclude that pDCs mediate early antiviral IFN-I responses and influence the accrual of virus-specific NK or CD8(+) T cells in a virus-dependent manner.

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Decreased Type I Interferon Production by Plasmacytoid Dendritic Cells Contributes to Severe Dengue.

Project description:The clinical presentation of dengue virus (DENV) infection is variable. Severe complications mainly result from exacerbated immune responses. Type I interferons (IFN-I) are important in antiviral responses and form a crucial link between innate and adaptive immunity. Their contribution to host defense during DENV infection remains under-studied, as direct quantification of IFN-I is challenging. We combined ultra-sensitive single-molecule array (Simoa) digital ELISA with IFN-I gene expression to elucidate the role of IFN-I in a well-characterized cohort of hospitalized Cambodian children undergoing acute DENV infection. Higher concentrations of type I IFN proteins were observed in blood of DENV patients, compared to healthy donors, and correlated with viral load. Stratifying patients for disease severity, we found a decreased expression of IFN-I in patients with a more severe clinical outcome, such as dengue hemorrhagic fever (DHF) or dengue shock syndrome (DSS). This was seen in parallel to a correlation between low IFNα protein concentrations and decreased platelet counts. Type I IFNs concentrations were correlated to frequencies of plasmacytoid DCs, not DENV-infected myloid DCs and correlated inversely with neutralizing anti-DENV antibody titers. Hence, type I IFN produced in the acute phase of infection is associated with less severe outcome of dengue disease.

| S-EPMC7773824 | biostudies-literature

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