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CD11c+ myeloid cell exosomes regulate intestinal inflammation

ABSTRACT: CD11c+ myeloid cell exosomes regulate intestinal inflammation

PROVIDER: PRJNA788743 | ENA |

REPOSITORIES: ENA

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CD11c+ myeloid cell exosomes regulate intestinal inflammation

Project description:Intercellular communication is critical for maintaining homeostasis in mammalian organ systems, including the gastrointestinal (GI) tract. Exosomes are small nanoscale lipid extracellular vesicles that mediate communication between a wide variety of cell types. Notably, the roles played by immune cell exosomes in regulating homeostasis and inflammation in the GI tract are largely uncharacterized. By generating novel mouse strains deficient in cell-specific exosome production, we demonstrate that specific disruption of exosome signaling via the deletion of Rab27a in myeloid cells exacerbates colitis, which is reversed through administration of dendritic cell (DC)-derived exosomes. Profiling small, non-coding RNAs within exosomes from colonic tissues revealed a distinct subset of microRNAs (miRNAs) carried by both colon- and DC-derived exosomes. Among the DC-enriched exosomal miRNAs, miR-146a was transferred from gut immune cells to myeloid and T cells through a Rab27-dependent mechanism to regulate macrophage phenotypes during colitis. Upon assessing clinical samples, RAB27A was also expressed at lower levels in a cohort of ulcerative colitis patients. Together, this work reveals an exosome-mediated regulatory mechanism underlying gut inflammation, and paves the way for potential use of exosomes containing miRNA cargo as a novel therapeutic for inflammatory bowel disease.

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IRF5 promotes intestinal inflammation by guiding monocyte differentiation towards pathogenic CD11c+ macrophage phenotype

Project description:IRF5 promotes intestinal inflammation by guiding monocyte differentiation towards pathogenic CD11c+ macrophage phenotype

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Project description:IRF5 promotes intestinal inflammation by guiding monocyte differentiation towards pathogenic CD11c+ macrophage phenotype [small_bulk_rnaseq]

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IRF5 promotes intestinal inflammation by guiding monocyte differentiation towards pathogenic CD11c+ macrophage phenotype [single_cell_rnaseq]

Project description:IRF5 promotes intestinal inflammation by guiding monocyte differentiation towards pathogenic CD11c+ macrophage phenotype [single_cell_rnaseq]

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Gene expression profile in CD11c+ splenic dendritic cells and CD11c+CD103+ dendritic cells from mesenteric lymph nodes (MLN) of mice with DC-specific targeting of TGFBR2

Project description:Transcriptome analysis of dentritic cells from the spleen (CD11c+) or MLN (CD11c+CD103+) of mice with DC-specific deletion of TGFBR2 gene, or their control littermates. TRGFR2 gene was deleted in dendritic cells using Cre/lox approach. Mice with this deletion develop spontaneous multi-organ autoimmune inflammation and die by 15 weeks of age. Splenic CD11c+ Dc were isolated by magetic cell sorting. MLN CD11c+CD103+ DC were flow sorted. RNA was isolated using RNAqueous-Micro kit (Ambion) and analyzed using Affymetrix Mouse Exon 1.0 ST Array

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IRF5 promotes intestinal inflammation by guiding monocyte differentiation towards pathogenic CD11c+ macrophage phenotype [small_bulk_rnaseq]

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