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Analysis of classical and migratory DC from the skin draining LNs of Flt3L treated mice and comparison to LPS treated DC from skin draining LN and peritoneal macrophages

ABSTRACT: Analysis of the differential transcriptome of DC derived from tissue vs. LN origin. The overall hypothesis is these data would reveal how migratory DC may be differently programmed from classical DC and might also suggest difference within migratory DC subsets relating to function.

ORGANISM(S): Mus musculus

PROVIDER: GSE53588 | GEO | 2014/08/01

SECONDARY ACCESSION(S): PRJNA232460

REPOSITORIES: GEO

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Analysis of classical and migratory DC from the skin draining LNs of Flt3L treated mice and comparison to LPS treated DC from skin draining LN and peritoneal macrophages

Project description:Analysis of the differential transcriptome of DC derived from tissue vs. LN origin. The overall hypothesis is these data would reveal how migratory DC may be differently programmed from classical DC and might also suggest difference within migratory DC subsets relating to function. RNA obtained from migratory DC subsets and classical CD8a DC isolated by flow cytometry sorting from skin draining LNs of Flt3L treated mice or LPS treated mice

2014-08-01 | E-GEOD-53588 | biostudies-arrayexpress

RNA-sequencing of mouse Lang+ and Lang- migratory dendritic cells (DC) under 2 pathogenic conditions of atopic dermatitis

Project description:Comparison of mouse Lang+ and Lang- migratory dendritic cells (DC) under 2 pathogenic conditions of atopic dermatitis (MC903-treated and OVA treated)

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scRNA-seq analysis of dendritic cells in skin draining lymph nodes of CLEC4C-DTR mice treated with FITC hapten

Project description:Skin draining lymph node dendritic cell populations are known to be diverse and distinguishable via their migratory or resident properties as well as by lineage. We analyzed these populations at steady state and during the sensitization phase of the Th2-driven FITC-hapten contact hypersensitivity (CHS) model. We also analyzed the dendritic cells populations of CLEC4C-DTR+ mice treated with diptheria toxin, which demonstrate exacerbated pathology in the FITC-CHS model. We demonstrate the diversity of dendritic cell populations at steady state and during type 2 inflammation, and surprisingly, reveal a skewing of the DC populations in DT treated CLEC4C-DTR+ mice, with an enrichment of DC2 migratory populations and depletion of CD326+ migratory cells in addition to pDC.

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A chemokine trail laid down by migratory dendritic cells directs antigen-presenting monocytes into draining lymph nodes

Project description:Antigen presenting dendritic cells (DCs) and monocytes capture and transport antigens from barrier tissues for presentation to antigen-specific T cells in the draining-lymph nodes (LNs). While DCs enter LNs through afferent lymphatics in a CCR7-dependent manner, how exactly antigen-carrying monocytes reach LNs is less clear since monocytes do not express CCR7 and can also enter LNs via the bloodstream. In steady state, and following injection of several PAMPs, scRNA-seq data on LN mononuclear phagocytes identified LN resident versus migratory type 1 and type 2 conventional (c)DCs despite downregulation of DC subset-defining transcripts, such as Xcr1, Clec9a, H2-Ab1, Sirpa, and Clec10a on migratory cDCs. Migratory cDCs gained expression of transcripts controlling cellular migration such as Ccr7, Ccl17, Ccl22, and Ccl5, while migratory monocytes expressed Ccr5 without Ccr7. Using two tracking methods and a gating strategy that clearly distinguishes migratory CD88hiCD26lo monocytes from CD88-CD26hi cDCs, we found that both captured antigens in the lung and migrated to lung-draining LNs. Using global and mixed-chimeric Ccl5-, Ccr2-, Ccr5-, Ccr7-, and Batf3-deficient mice, we found that CCR5+ monocytes follow CCL5-secreting migratory cDCs to reach the draining LN via lymphatic vessels. In a model of asthma, such recruited monocytes regulated the induction of type 2 immunity. Overall, our data suggest that CCL5-secreting migratory cDCs lay down the chemokine trail for CCR5+ antigen-presenting monocytes to reach draining lymph nodes and regulate adaptive immunity.

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HDAC inhibition by TSA and Butyrate In Flt3L-elicited DC

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Migratory dendritic cells in skin-draining lymph nodes have nickel-binding capabilities.

Project description:Nickel (Ni) is the most frequent metal allergen and induces Th1-dependent type-IV allergies. In local skin, epidermal Langerhans cells (LCs) and/or dermal dendritic cells (DCs) uptake antigens and migrate to draining lymph nodes (LNs). However, the subsets of antigen-presenting cells that contribute to Ni presentation have not yet been identified. In this study, we analyzed the Ni-binding capabilities of murine DCs using fluorescent metal indicator Newport Green. Elicitation of Ni allergy was assessed after intradermal (i.d.) injection of Ni-treated DCs into ear pinnae of Ni-sensitized mice. The Ni-binding capabilities of MHC class IIhi CD11cint migratory DCs were significantly stronger than those of MHC class IIint CD11chi resident DCs and CD11cint PDCA1+ MHC class IIint B220+ plasmacytoid DCs. Migratory DCs in skin-draining and mandibular LNs showed significantly stronger Ni-binding capabilities than those in mesenteric and medial iliac LNs. An i.d. injection of IL-1β induced the activation of LCs and dermal DCs with strong Ni-binding capabilities. Ni-binding LCs were detected in draining LNs after i.d. challenge with IL-1β and Ni. Moreover, an i.d. injection of Ni-treated DCs purified from skin-draining LNs elicited Ni-allergic inflammation. These results demonstrated that migratory DCs in skin-draining LNs have strong Ni-binding capabilities and elicit Ni allergy.

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single cell RNA sequencing of migratory dendritic cells after intranasal adjuvant/tolerogen administration

Project description:We compared migratory DCs in draining mediastinal lymph node after intranasal administration of different vaccine adjuvants based on CTA1 subunit of cholera toxin. The goal was to determine different characteristics of dendritic cells subsets after pro-inflammatory vs tolerogenic adjuvant. We had 3 groups: CTA1-DD (pro- inflammatory), CTA1(R7K)-DD (tolerogenic) and PBS to define DC which migrate to LN. All vaccine constructs included 3Ea peptide to allow for sorting of DC which took up the vaccine.

2023-05-15 | E-MTAB-12942 | biostudies-arrayexpress

Migratory CD11b+ conventional dendritic cells induce T follicular helper cell dependent antibody responses

Project description:T follicular helper (Tfh) cells are a subset of CD4+ T cells that promote antibody production during vaccination. Conventional dendritic cells (cDCs) efficiently prime Tfh cells; however, conclusions regarding the nature of the cDC responsible for instructing Tfh cell differentiation have differed between recent studies. We found that these discrepancies might exist, in part, due to the unusual sites used for immunization in murine models, which differentially bias which DC subsets access antigen. We used intranasal immunization as a physiologically relevant route of exposure that we show delivers antigen to all tissue DC subsets. Using a combination of mice in which the function of individual DC subsets is impaired and different formulations of antigen delivery, we determined that CD11b+ migratory type 2 conventional DCs (cDC2s) are necessary and sufficient for Tfh induction. DC-specific deletion of the guanine nucleotide exchange factor DOCK8 resulted in an isolated loss of CD11b+ cDC2 but not CD103+ cDC1 migration to lung-draining lymph nodes. Impaired cDC2 migration or development in DC-specific Dock8 or Irf4 knockout mice, respectively, led to reduced Tfh cell and antibody development, whereas loss of CD103+ cDC1s in Batf3-/- mice did not. Loss of cDC2-mediated Tfh responses was associated with impaired antibody-mediated protection from live influenza virus challenge. We show that migratory cDC2s uniquely carry antigen into the sub-anatomic regions of the lymph node where Tfh cell priming occurs, the T-B border. This work identifies the DC responsible for Tfh cell-dependent antibody responses, in particular when antigen dose is limiting or is encountered at a mucosal site, which could ultimately inform the formulation and delivery of vaccines.

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Armatimonadetes bacterium DC isolate:DC

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RNA-seq of Arc/Arg3.1-positive versus Arc/Arg3.1-negative skin migratory dendritic cells from healthy mice

Project description:The key function of migratory dendritic cells (migDCs) is to take up antigens in peripheral tissues and migrate to draining lymph nodes (dLN) to initiate immune responses. Recently, we discovered in mice that in the immune system activity-regulated cytoskeleton associated protein/activity-regulated gene 3.1 (Arc/Arg3.1) is exclusively expressed by migDCs and is a central driver of fast inflammatory migration. However, the frequency of Arc/Arg3.1 expressing cells in different migDC subsets including Langerhans cells (LC), their phylogenetic origin, transcription factor dependency and functional role remains unclear. Here we found that Arc/Arg3.1+ migDCs derived from common DC precursors (CDPs) and radio-resistant LCs. They were present in all migDC subsets and showed a consistent superiority in inflammatory migration but were independent of the transcription factors Irf4 or Batf3. In intradermal Staphylococcus aureus infection, a model that relies on effective inflammatory antigen transport, Arc/Arg3.1 deletion strongly reduced T cell responses. By contrast, Arc/Arg3.1 deficiency did not hamper the immune response to systemic Listeria monocytogenes infection, which does not require antigen transport. Thus, our results show that Arc/Arg3.1 is a molecular marker for defining a population of DCs with superior migratory capacity that spans across all migDC subsets irrespective of ontogeny and phenotype.

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