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Single-cell RNA sequencing reveals tissue-associated fibroblastic reticular cell heterogeneity in human secondary lymphoid organs

ABSTRACT: Single-cell RNA sequencing reveals tissue-associated fibroblastic reticular cell heterogeneity in human secondary lymphoid organs

PROVIDER: PRJNA796276 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17552855_1.fastq.gz	Fastqsanger.gz
	SRR17552855_2.fastq.gz	Fastqsanger.gz
	SRR17552856_1.fastq.gz	Fastqsanger.gz
	SRR17552856_2.fastq.gz	Fastqsanger.gz
	SRR17552857_1.fastq.gz	Fastqsanger.gz

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Single-cell RNA sequencing reveals tissue-associated fibroblastic reticular cell heterogeneity in human secondary lymphoid organs

Project description:Fibroblastic reticular cells (FRCs) actively support secondary lymphoid organ (SLO) architecture. They regulate innate and adaptive immunity by compartmentalizing immune cells in specialized niches, and tightly interacting with them. The phenotypic and functional diversity of FRCs in human SLOs remains largely uncharacterized. We performed a comprehensive profiling of FRCs by single-cell RNA sequencing on human tonsils and lymph nodes. We provide the first complete description of the tonsillar CD45-negative compartment. We identified and validated in tonsil, a population of follicular dendritic cells restricted to the mantle zone and discovered two CCL21-negative FRC subsets intermingling with T-cell zone reticular cells in the extrafollicular space. We also identified podoplanin-positive epithelial cells as a potential plasma cell (PC) niche. We found two levels of FRC-associated diversity: i) tissue-specific subsets; ii) shared subsets with tissue-specific gene signatures. These findings shed new light on the role of FRCs in supporting SLO-specific immune responses.

2023-02-01 | GSE193449 | GEO

Intestinal fibroblastic reticular cell niches control innate lymphoid cell homeostasis and function - Innate lymphoid cells

Project description:Innate lymphoid cells (ILC) in the small intestine govern immune homeostasis and protect the host against gut pathogens. While distinct cell-intrinsic signals have been identified that determine ILC development and differentiation, it has remained unclear which cell population regulates ILC sustenance. Using unbiased single cell RNA transcriptomic analysis of intestinal fibroblasts, we have identified a specialized Ccl19-expressing fibroblastic reticular cell (FRC) population that underpins solitary intestinal lymphoid tissue (SILT) structures including cryptopatches and isolated lymphoid follicles. Conditional ablation of lymphotoxin-β receptor (LTβR) signalling in SILT FRC impeded the maturation of isolated lymphoid follicles and blocked ILC maintenance through the downregulation of IL-7, consequently resulting in the elevated susceptibility to bacterial infection. Moreover, specific Ltbr ablation in FRC during adulthood revealed that constant LTβR-dependent FRC-ILC interaction is required to maintain SILT structures and ILC populations. Taken together, our study unveils a critical intestinal FRC niche that secures protective gut immunity.

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Intestinal fibroblastic reticular cell niches control innate lymphoid cell homeostasis and function - Intestinal fibroblasts

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Intestinal fibroblastic reticular cell niches control innate lymphoid cell homeostasis and function - Innate lymphoid cells

Project description:Intestinal fibroblastic reticular cell niches control innate lymphoid cell homeostasis and function - Innate lymphoid cells

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Single cell RNAseq of B cell interacting reticular cells and immune cells from murine secondary lymphoid organs

Project description:B cell-interacting reticular cells (BRC) form transcriptionally and topologically stable immune-interacting microenvironments that direct efficient humoral immunity. While several immune niche factors have been elucidated, the cues sustaining BRC function and topology across activation states remain unclear. Here, we employed single cell RNA-sequencing of stromal cells and immune cells from murine lymph nodes, Peyer’spatches and spleens to analyse local BRC-immune cell interactions and compare them across SLOs and species. Shared BRC subsets were imprinted by tissue-specific gene signatures, but also expressed functionally convergent niche factors that directed regionalized leukocyte composition. Local BRC-immune cell interactions sustained BRC subset identity via immune cell-provided maturation factors. Bidirectional signalling programs were independent of activation state and mirrored across murine and human tissues. Collectively, our data reveal a conserved set of feedforward BRC-immune cell circuits that sustain topologically-organized, functional niches across inflammatory states, lymphoid organs and species.

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Type I interferon signaling in fibroblastic reticular cells prevents exhaustive activation of antiviral CD8+ T cells

Project description:Fibroblastic reticular cells (FRC) shape the organization of secondary lymphoid organs and actively promote the induction of immune responses by coordinating the interaction of innate and adaptive immune cells. However, the mechanisms underlying FRC functions during viral infections have remained largely unexplored. In the study, we combined FRC-specific genetic ablation of the type 1 IFN-alpha receptor (IFNAR) with high-dimensional transcriptomics analyses to elaborate the phenotypical alterations and functional consequences of impaired innate immunological sensing in FRC during lymph node-restricted viral infection

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Activation of TLR9 signaling suppresses the immuno modulating functions of CD55lo fibroblastic reticular cells during bacterial peritonitis

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Project description:Immune protection of the body cavities depends on the swift activation of innate and adaptive immune responses in non-classical secondary lymphoid organs known as fat-associated lymphoid clusters (FALCs). While it is well-established that fibroblastic reticular cells (FRCs) are an integral component of the immune-stimulating infrastructure of lymph nodes and other classical secondary lymphoid organs, it has remained elusive whether and how FRCs in FALCs contribute to peritoneal immunity. Using FRC-specific gene targeting, we found that FALCs are underpinned by an elaborated FRC network and that initiation of peritoneal immunity was governed through FRC activation via MyD88-dependent innate immunological sensing. FRC-specific ablation of Myd88 expression blocked recruitment of inflammatory monocytes into FALCs and subsequent CD4+ T cell-dependent B-cell activation. Moreover, containment of Salmonella infection was compromised in conditionally Myd88-deficient mice indicating that FRCs in FALCs function as initial checkpoint in the orchestration of protective immune responses in the peritoneal cavity.

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Aldh1a2+ fibroblastic reticular cells regulate lymphocyte recruitment in omental milky spots

Project description:Milky spots, lymphoid clusters present in visceral adipose tissue omentum, play central roles in the regulation of abdominal immunity. Milky spots exhibit hybrid nature between secondary lymph organs and ectopic lymphoid tissues, yet the mechanism of their development and maturation is poorly understood. Here, we identified a subset of fibroblastic reticular cells (FRCs) that are uniquely present in omental milky spots. These FRCs were characterized by the expression of retinoic acid converting enzyme, Aldh1a2, and endothelial cell marker, Tie2, in addition to canonical FRC-associated genes. Diphtheria toxin-mediated ablation of Aldh1a2+ FRCs resulted in the alteration in milky spot structure with a significant reduction in size and cellularity. Mechanistically, Aldh1a2+ FRCs regulated the display of chemokine CXCL12 on high endothelial venules (HEVs), which recruit blood-borne lymphocytes from circulation. We further found that Aldh1a2+ FRCs are required for the maintenance of peritoneal lymphocyte composition. These results illustrate the homeostatic roles of FRCs in the formation of non-classical lymphoid tissues.

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Aldh1a2+ fibroblastic reticular cells regulate lymphocyte recruitment in omental milky spots (single cell RNA-Seq)

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