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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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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

PRC2 preserves cellular plasticity and restricts intestinal secretory lineage commitment

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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.

2017-04-19 | PXD006251 | Pride

IL-21 restricts virus-driven Treg cell expansion in chronic LCMV infection.

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

Project description:The accumulation of acidic metabolic waste products within the tumor microenvironment profoundly inhibits effector functions of tumor-infiltrating lymphocytes (TILs). However, it is unclear whether extracellular-acidosis impacts T cell metabolic fitness and differentiation status. Here, we surprisingly found that prolonged acid exposure reprogrammed T cell intracellular metabolism and mitochondrial fitness, and preserved T cell stemness. Elevated extracellular-acidosis impaired methionine uptake and metabolism via downregulating SLC7A5, therefore altering H3K27me3 deposition at the promoters of crucial T cell stemness genes. These changes promoted the maintenance of a “stem-like memory” state and improved long-term in vivo persistence and anti-tumor efficacy. Our findings not only reveal the unexpected roles of extracellular-acidosis in the maintenance of stem-like properties of T cells, but also advance our understanding of the direct involvement of methionine metabolism in T cell stemness.

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Project description:Slc20a1b is essential for hematopoietic stem/progenitor cell expansion in zebrafish

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NK cell expansion on uAPC helper cells

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Slc20a1b is essential for hematopoietic stem/progenitor cell expansion in zebrafish

Project description:Hematopoietic stem and progenitor cells (HSPCs) are able to self-renew and can give rise to all blood lineages throughout their lifetime, yet the mechanisms regulating HSPC development have yet to be discovered. In this study, we characterized a hematopoiesis defective zebrafish mutant line named smu07, which was obtained from our previous forward genetic screening, and found the HSPC expansion deficiency in the mutant. Positional cloning identified that slc20a1b, which encodes a sodium phosphate cotransporter, contributed to the smu07 blood phenotype. Further analysis demonstrated that mutation of slc20a1b affects HSPC expansion through cell cycle arrest at G2/M phases in a cell-autonomous manner. Our study shows that slc20a1b is a vital regulator for HSPC proliferation in zebrafish early hematopoiesis and provides valuable insights into HSPC development.

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Glutathione restricts serine metabolism to preserve regulatory T cell function

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