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Inflammatory Type 2 cDCs Acquire Features of cDC1s and Macrophages to Orchestrate Immunity to Respiratory Virus Infection (scRNA-Seq)

ABSTRACT: Inflammatory Type 2 cDCs Acquire Features of cDC1s and Macrophages to Orchestrate Immunity to Respiratory Virus Infection (scRNA-Seq)

PROVIDER: PRJNA629368 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11647753.fastq.gz	Fastqsanger.gz
	SRR11647754.fastq.gz	Fastqsanger.gz
	SRR11647755.fastq.gz	Fastqsanger.gz
	SRR11647756.fastq.gz	Fastqsanger.gz

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Inflammatory Type 2 cDCs Acquire Features of cDC1s and Macrophages to Orchestrate Immunity to Respiratory Virus Infection

Project description:Inflammatory Type 2 cDCs Acquire Features of cDC1s and Macrophages to Orchestrate Immunity to Respiratory Virus Infection

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Inflammatory Type 2 cDCs Acquire Features of cDC1s and Macrophages to Orchestrate Immunity to Respiratory Virus Infection (microarray)

Project description:Inflammatory Type 2 cDCs Acquire Features of cDC1s and Macrophages to Orchestrate Immunity to Respiratory Virus Infection (microarray)

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Inflammatory Type 2 cDCs Acquire Features of cDC1s and Macrophages to Orchestrate Immunity to Respiratory Virus Infection.

Project description:The phenotypic and functional dichotomy between IRF8+ type 1 and IRF4+ type 2 conventional dendritic cells (cDC1s and cDC2s, respectively) is well accepted; it is unknown how robust this dichotomy is under inflammatory conditions, when additionally monocyte-derived cells (MCs) become competent antigen-presenting cells (APCs). Using single-cell technologies in models of respiratory viral infection, we found that lung cDC2s acquired expression of the Fc receptor CD64 shared with MCs and of IRF8 shared with cDC1s. These inflammatory cDC2s (inf-cDC2s) were superior in inducing CD4+ T helper (Th) cell polarization while simultaneously presenting antigen to CD8+ T cells. When carefully separated from inf-cDC2s, MCs lacked APC function. Inf-cDC2s matured in response to cell-intrinsic Toll-like receptor and type 1 interferon receptor signaling, upregulated an IRF8-dependent maturation module, and acquired antigens via convalescent serum and Fc receptors. Because hybrid inf-cDC2s are easily confused with monocyte-derived cells, their existence could explain why APC functions have been attributed to MCs.

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Inflammatory Type 2 cDCs Acquire Features of cDC1s and Macrophages to Orchestrate Immunity to Respiratory Virus Infection (microarray)

Project description:The phenotypic and functional dichotomy between IRF8+ type 1 and IRF4+ type 2 conventional dendritic cells (cDC1-cDC2) is well accepted; it is unknown how robust this dichotomy is under inflammatory conditions, when additionally monocyte-derived cells (MCs) become competent antigen presenting cells (APC). Using single-cell technologies in models of respiratory viral infection, we found that lung cDC2s acquired expression of Fc receptor CD64 shared with MCs, and of IRF8 shared with cDC1s. These inflammatory (Inf-)cDC2s were superior in inducing CD4+ T helper (Th) cell polarization while simultaneously presenting antigen to CD8+ T cells. When carefully separated from inf-cDC2s, MCs lacked APC function. Inf-cDC2 matured in response to cell-intrinsic toll-like receptor and type 1 interferon receptor signaling, upregulated an IRF8-dependent maturation module and acquired antigens via convalescent serum and Fc receptors. Since hybrid inf-cDC2s are easily confused with monocyte-derived cells, their existence could explain why APC functions have been attributed to MCs.

2020-05-08 | GSE149618 | GEO

Inflammatory Type 2 cDCs Acquire Features of cDC1s and Macrophages to Orchestrate Immunity to Respiratory Virus Infection (scRNA-Seq)

2020-05-08 | GSE149617 | GEO

Inflammatory Type 2 cDCs Acquire Features of cDC1s and Macrophages to Orchestrate Immunity to Respiratory Virus Infection

Project description:This SuperSeries is composed of the SubSeries listed below.

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Expression data from WT cDC1s, Zeb2 KO cDC1s, Nfil3 Zeb2 DKO cDC1s and Zeb2 Id2 DKO cDC1s

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Gene expression in WT, Flt3 KO, and Flt3L KO cDC1s and cDC2s

Project description:The goal of this study was to determine whether there are any gene expression changes in cDC1s and cDC2s from WT, Flt3 KO, or Flt3L KO mice. Specifically whether developing in the absence of Flt3 signaling had any effects on the gene expression of the cDCs

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Expression data from WT cDC1s, Zeb2 KO cDC1s, Nfil3 Zeb2 DKO cDC1s and Zeb2 Id2 DKO cDC1s

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Project description:Immune tolerance is an active state of unresponsiveness of the immune system to antigens (Ags) that have the potential to induce an immune response1. Such tolerance is beneficial in avoiding autoimmunity and rejection of organ transplants, but detrimental in cancer2. Type 1 conventional dendritic cells (cDC1s) are unique in their efferocytosis3 and cross-presenting abilities4, resulting in T cell-mediated immunity5 or tolerance6-10. However, the mechanisms underlying the tolerogenic function of cDC1s remain largely unknown. Here, we show that the erythropoietin receptor (EpoR) acts as a critical switch that determines the tolerogenic state of cDC1s and the threshold of Ag-specific T cell responses. In total lymphoid irradiation-induced allograft tolerance11,12, EpoR+ cDC1s induce donor-specific CD4+FoxP3+ regulatory T cells (Tregs), and conditional knockout of EpoR in cDC1s abrogates Ag-specific Treg induction, resulting in allograft rejection. In the steady state, EpoR+ migratory cDC1s control Ag-specific Treg induction in peripheral lymph nodes (LNs). In cancer, EpoR is expressed on both tumor Ag-carrying, tumor-infiltrating cDC1s, as well as migratory cDC1s in tumor-draining LNs (tdLNs). Loss of EpoR from cDC1s leads to tumor reduction by enhancing tumor Ag-specific CD8+ T cell priming and generating more precursor exhausted T cells13 in tdLNs, preserving CD8+ T cell precursor-like features and effector function, and reducing Tregs in the tumor. Thus, targeting EpoR on cDC1s to induce or inhibit immune tolerance should enable new ways to treat a variety of diseases.

2024-03-01 | GSE253056 | GEO

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