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C5aR+ lysozyme-expressing dendritic cells (LysoDCs) comprise a unique cell population in the Peyer’s patch (PP) subepithelial dome (SED).

ABSTRACT: C5aR+ lysozyme-expressing dendritic cells (LysoDCs) comprise a unique cell population in the Peyer’s patch (PP) subepithelial dome (SED).

PROVIDER: PRJNA577913 | ENA |

REPOSITORIES: ENA

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C5aR+ lysozyme-expressing dendritic cells (LysoDCs) comprise a unique cell population in the Peyer’s patch (PP) subepithelial dome (SED).

Project description:CD11chi cells can be subdivided into six different cell subsets:plasmacytoid DCs (pDCs), CD8a+ DCs, CD11b+ DCs, double-negative (DN) DCs, LysoDCs, and LysoMacs. Among these, LysoDC (CD4–) and LysoMacs (CD4+) are classified as CD11chiMHC class II+BST2intSIRPαhi lysozyme+ cells, depending on whether they express CD4. Here, we determine that C5aR expressed in LysoDC and LysoMacs. We used microarrays to determine the lineage of C5aR+ LysoDC and C5aR- LysoDC.

2021-04-12 | GSE138973 | GEO

Gene expression data of Peyer's patch LysoDC differentiation states and macrophages at steady state and under TLR7 ligand stimulation

Project description:The specialized monocyte-derived phagocytes termed LysoDC are hallmarks of Peyer’s patches where their main function is to sample pathogens. However, their differentiation pathway and migratory properties remain uncharacterized. From single-cell RNA sequencing, we built LysoDC differentiation trajectories and fate diversity in correlation with their location and functions. All LysoDC differentiation states display similar phagocytic activity. One of them is located in follicles in a CXCR5-independent manner whereas the others reside in subepithelial domes (SED) and mature as they get closer to the epithelium. Immature LysoDC proliferate. Mature LysoDC acquire a gene signature shared with SIRP alpha-expressing conventional DC and prime naïve T cells in vitro but, at steady state, do not migrate in naïve T cells-enriched interfollicular regions (IFR). However, upon stimulation, they express the chemokine receptor CCR7 and migrate from the SED to the IFR periphery where they strongly interact with proliferative T cells. Finally, we show that LysoDC populates human Peyer’s patches.

2020-01-08 | GSE133864 | GEO

Double-negative B cells and DNASE1L3 colocalise with microbiota in gut-associated lymphoid tissue

Project description:Intestinal homeostasis is maintained by the response of gut-associated lymphoid tissue to bacteria transported across the follicle associated epithelium into the subepithelial dome. The initial response to antigens and how bacteria are handled is incompletely understood. By iterative application of spatial transcriptomics and multiplexed single-cell technologies, we identify that the double negative 2 subset of B cells, previously associated with autoimmune diseases, is present in the subepithelial dome in health. We show that in this location double negative 2 B cells interact with dendritic cells co-expressing the lupus autoantigens DNASE1L3 and C1q and microbicides. We observe that in humans, but not in mice, dendritic cells expressing DNASE1L3 are associated with sampled bacteria but not DNA derived from apoptotic cells. We propose that fundamental features of autoimmune diseases are microbiota-associated, interacting components of normal intestinal immunity.

2024-03-28 | GSE251693 | GEO

C5aR+ dendritic cells fine-tune the Peyer’s patch microenvironment to induce antigen-specific CD8+ T cells

Project description:The mucosa is an ideal route for vaccination against pathogen infection, but the effective adjuvant capable of overcoming the tolerogenic dendritic cell (DC) environment is unavailable. We characterized type 2 conventional DCs and lysozyme-expressing monocyte-derived DCs (LysoDCs) of Peyer’s patches to identify the vaccination target cells through single-cell RNA sequencing. Based on functional analysis of the data, we suggest that C5aR+ LysoDCs and Co1 peptide, a C5aR ligand, as a target cell and an adjuvant, respectively, for mucosal vaccination. Co1-mediated stimulation of C5aR+ LysoDCs increased the level of reactive oxygen species, leading to CCL3-mediated chemotaxis and exogenous antigen cross-presentation, which elicited an antigen-specific CD8+ T cell response. In a SARS-CoV-2 vaccine model, Co1 peptide increased the frequency of antigen-specific polyfunctional CD8+ T cells in systemic as well as mucosal compartments. Collectively, LysoDC activation by Co1 peptide potentiates vaccination efficiency by constructing an immunostimulatory environment in the mucosal immune inductive site.

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Peyer’s Patch Germinal Centers Select Innate-like BCRs

Project description:Peyer’s Patch Germinal Centers Select Innate-like BCRs

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Peyer’s patches are required for Bacteroides fragilis to induce protective systemic IgA

Project description:Gut-educated IgA-secreting plasma cells that disseminate beyond the mucosa and into systemic tissues can help prevent disease in several contexts. Here we show, the commensal bacteria Bacteroides fragilis (Bf), is an efficient inducer of systemic IgA responses. The generation of bone marrow IgA plasma cells and high levels of serum IgA specific to Bf requires robust intestinal colonization. Bf-specific IgA responses were severely diminished in mice lacking Peyer’s patches, but not mice lacking a cecal patch. Colonization resulted in few changes in the host transcriptional profile in the gut, suggesting a commensal relationship. High levels of Bf-specific serum IgA, but not IgG, provided protection from peritoneal abscess formation in a bowel perforation model of Bf dissemination. These findings demonstrate a critical role for bacterial colonization and Peyer’s patches in the induction of robust systemic IgA responses that confer protection from bacterial dissemination originating from the gut.

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Neutrophil extracellular traps melt Peyer’s patches following stroke and myocardial infarction

Project description:Sterile tissue injury after stroke causes lymphocyte contraction in lymphoid tissues and may decrease circulating IgA-levels. Intestinal Peyer’s patches (PP) harbor large numbers of IgA+ B cell precursors and plasma cells. Whether and how tissue injury triggers PP-B cell death, thereby mediating IgA-loss, is unknown. We found decreased circulating IgA levels in stroke and myocardial infarction patients. Experimental stroke and myocardial infarction in mice phenocopied the human situation. Decreased plasma and fecal IgA were accompanied by rapid and macroscopic shrinkage of PP caused by substantial losses of PP-resident IgA+ precursors and plasma cells in mice. Tissue injury induced neutrophil activation endowed with the release of toxic neutrophil extracellular traps (NETs). Antibody-mediated or genetically- induced neutrophil loss, digestion of NETs, or inhibition of their release by the Gasdermin D blockade completely prevented lymphocyte loss and PP shrinkage. We also identified NETs in the plasma of stroke and myocardial infarction patients. Hence, tissue injury induces systemic NET-release, which might be targeted to maintain immune homeostasis at mucosal barriers.

2024-02-28 | PXD044644 | Pride

Fibroblastic reticular cell lineage convergence in Peyer’s patches governs intestinal homeostasis

Project description:Fibroblastic reticular cell lineage convergence in Peyer’s patches governs intestinal homeostasis

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