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IL-10 Signaling Restricts Murine Progenitor Cell Expansion and Preserves Stem Cell Function

ABSTRACT: IL-10 Signaling Restricts Murine Progenitor Cell Expansion and Preserves Stem Cell Function

PROVIDER: PRJNA779936 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16928944_1.fastq.gz	Fastqsanger.gz
	SRR16928944_2.fastq.gz	Fastqsanger.gz
	SRR16928945_1.fastq.gz	Fastqsanger.gz
	SRR16928945_2.fastq.gz	Fastqsanger.gz
	SRR16928946_1.fastq.gz	Fastqsanger.gz

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IL-10 Signaling Restricts Murine Progenitor Cell Expansion and Preserves Stem Cell Function

Project description:Inflammation causes increased signaling and proliferation in hematopoietic stem and progenitor cells (HSPCs), but the specific role of anti-inflammatory cytokines such as IL-10 on HSPCs is less clear. Using IL-10 receptor (IL-10R)-deficient mice we observed an increased frequency and number of HSPCs in the bone marrow (BM) relative to wild-type (WT) mice with an increased frequency of mature myeloid cells. Consistent with this, we observed reduced expansion of WT lineage-negative HSPCs after in vitro exposure to IL-10 with a specifically pronounced suppression of MPP2 cells. This reduced expansion was not observed with IL-22 or IFN-λ2, cytokines which signal through receptors that also contain the IL-10 receptor common β chain or with HSPCs from Il10ra-/- mice. To understand the mechanism of reduced expansion of MPP2 cells and preserved HSC numbers in mice with intact IL-10 signaling, we stimulated FACS-purified WT cells with IL-10 and performed expression analysis. IL-10 stimulation of HSCs increased the non-canonical Wnt pathway gene Wnt4 which is implicated in HSC quiescence and long-term function. In contrast, IL-10 stimulation in MPP2 cells modulated the TGFβ pathway and increased the expression of E2f5, a transcription factor that negatively regulates proliferation. Taken together, this study reveals a previously unrecognized role for IL-10 in suppressing HSPC cell expansion and promoting HSC function.

2021-11-19 | GSE188677 | GEO

Extracellular-acidosis restricts one-carbon metabolism and preserves T cell stemness

Project description:Extracellular-acidosis restricts one-carbon metabolism and preserves T cell stemness

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Extracellular-acidosis restricts one-carbon metabolism and preserves T cell stemness: CUT&Tag

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Extracellular-acidosis restricts one-carbon metabolism and preserves T cell stemness: RNA-seq

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PRC2 preserves cellular plasticity and restricts intestinal secretory lineage commitment

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Maternal IL-10 restricts fetal emergency myelopoiesis

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Ndfip1 restricts mTORC1 signalling and glycolysis in regulatory T cells to prevent autoinflammatory disease

Project description:Project abstract: Foxp3+ T regulatory (Treg) cells have important functions in suppressing immune cell activation and establishing normal immune homeostasis. How Treg cells maintain their identity is not completely understood. Here we show that Ndfip1, a co-activator of Nedd4-family E3 ubiquitin ligases, is required for Treg cell stability and function. Ndfip1 deletion in Treg cells disrupts immune homeostasis and results in autoinflammatory disease. Ndfip1-deficient Treg cells are highly proliferative and are more likely to lose Foxp3 expression to become IL-4-producing TH2 effector cells. Proteomic analyses indicate that Ndfip1 deficiency alters the metabolic signature of Treg cells. Metabolic profiling reveals elevated glycolysis and increased mTORC1 signalling. Additional data suggest that Ndfip1 restricts Treg cell metabolic capacity and IL-4 production via distinct mechanisms. Thus, Ndfip1 preserves Treg lineage stability by preventing the expansion of highly proliferative and metabolically active cells that can cause immunopathology via secretion of IL-4.

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Extracellular-acidosis restricts one-carbon metabolism and preserves T cell stemness (RNA-seq of sodium lactate samples)

Project description:Extracellular-acidosis restricts one-carbon metabolism and preserves T cell stemness (RNA-seq of sodium lactate samples)

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IL-10 restricts memory T cell inflation during cytomegalovirus infection.

Project description:The beta-herpesvirus CMV induces a substantial and progressive expansion of virus-specific memory CD8 T cells, which protect the host against viral reactivation from latency. In this paper, we report that this expansion, or "inflation," of memory T cells is amplified dramatically during mouse CMV infection of IL-10 knockout (IL-10(-/-)) mice. T cells from IL-10(-/-) mice were oligoclonal, exhibited a highly activated phenotype, expressed antiviral cytokines, and degranulated in response to cognate Ag encounter ex vivo. Moreover, latent viral load was reduced in IL-10(-/-) mice. Importantly, these results were recapitulated by IL-10R blockade during chronic/latent infection of wild-type mice. These data demonstrate that regulatory immune mechanisms can influence CMV-specific T cell memory and suggest a possible rationale for the acquisition of functional IL-10 orthologs by herpesviruses.

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