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Immunoregulatory function of peripheral blood CD71+ erythroid cells in pediatric inflammatory diseases

ABSTRACT: Immunoregulatory function of peripheral blood CD71+ erythroid cells in pediatric inflammatory diseases

PROVIDER: PRJNA688921 | ENA |

REPOSITORIES: ENA

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Immunoregulatory function of peripheral blood CD71+ erythroid cells in pediatric inflammatory diseases

Project description:Human CD71+ erythroid cells (CECs) have been recognized to have an immunoregulatory function via direct cell-cell interaction and soluble mediators such as arginase-2 and reactive oxygen species. Circulating CECs increase in healthy newborns or patients with hemolytic, malignant and cardiopulmonary disorders. To assess the pathophysiological role of CECs in inflammatory diseases, we studied the gene expression and function focusing on systemic-onset juvenile idiopathic arthritis (SoJIA). Peripheral blood mononuclear cells obtained from patients with SoJIA expressed upregulated erythropoiesis-related genes, that determined the largest increase of circulating CECs during active phase SoJIA of all inflammatory diseases including polyarthritis, Kawasaki disease, bacteremia and systemic lupus erythematosus. Despite the opposite roles of erythropoietin and hepcidin in erythropoiesis, both serum levels positively correlated with the amounts of peripheral blood CECs in SoJIA patients. There were positive correlations between CECs and inflammatory markers of C-reactive protein, interleukin (IL)-6, IL-18, or soluble TNF receptor. Co-culture with active SoJIA-driven CECs significantly suppressed the secretion of IL-1β, IL-6, and IL-8 from healthy donor monocytes. The top of upregulated genes in SoJIA-driven CECs was ARG2 compared with those in CECs from cord blood controls. On the other hand, cytokine productions from monocytes were suppressed by co-culture even with an arginase inhibitor. CECs are mobilized to periphery in SoJIA for the control of excessive inflammation via the immuno-regulatory pathways partly involving arginase-2. Understanding the association between CECs and magnitude of systemic inflammation may clarify the unappreciated role of erythroid precursors in health and disease process of immune dysregulation.

2021-07-20 | GSE164120 | GEO

CD71+ HSC/MPP

Project description:We describe the unique enrichment of erythroid-megakaryocyte primed CD71+ phenotypic HSC/MPPs in steady-state PB.

2021-12-17 | GSE191084 | GEO

miRNA expression profiles of erythroid cells following hydroxyurea treatment for sickle cell anemia

Project description:We hypothesized that miRNA regulation may be invloved in hydroxyurea-mediated fetal hemoglobin induction. Microarray analysis was utilized as an initial screening tool to determine differential miRNA expression in CD71+ erythroid cells comparing cells from control individuals without sickle cell anemia to patients with sickle cell anemia prior to treatment with hydroxyurea and patients receiving the maximum tolerated dose (MTD) of hydroxurea. CD71+ cells were isolated from whole blood of control individuals (n=2), pediatric patients without hydroxyurea treatment (n=3) and pediatric patients at hydroxyurea MTD (n=3). All 8 samples were analyzed for miRNA expression.

2011-11-21 | E-GEOD-32035 | biostudies-arrayexpress

Identification of genes regulated by Rcor1 in CD71+, TER119- erythroid progenitors using mRNA-seq analysis

Project description:Transcription cofactor Rcor1 has been linked biochemically both to neurogenesis and hematopoiesis. Here we studied the function of Rcor1 in vivo and showed it is essential to erythropoeisis during embryonic development. Rcor1 mutant proerythroblasts, unlike normal cells, can form myeloid colonies in vitro. To investigate the underlying molecular mechanisms for block of erythropoiesis and increased myeloid potential, we used RNA-seq to reveal the differentially expressed genes from erythroid progenitors due to depletion of Rcor1. RNA were extracted from FACS sorted CD71+,TER119- erythroid progenitors from control (Rcor1+/+ and Rcor1+/-) or Mutant (Rcor1-/- ) E13.5 fetal liver. Each library was made by pooling RNA from several fetal livers. Two biological replicates were made for either control or mutant condition.

2014-06-03 | E-GEOD-50708 | biostudies-arrayexpress

Comprehensive analysis of human proteomic erythroid progenitors

Project description:CD34-positive cells from peripheral blood were culture for 5 days in erythroid differentiating medium. Four progenitor stages were sorted by FACS using the established cell surface markers CD34 and CD36 with CD117, CD71, and CD105 (Yan H, Am J Hematol, 2021). A comprehensive analysis of the proteome of these four erythroid progenitor stages was done in quadruplicate using a label free proteomic approach.

2023-10-30 | PXD042615 | Pride

RNA-seq on Enasidenib or DMSO Treated CD71+ Cells from Umbilical Cord Blood (UCB)

Project description:We aim to identify differentially expressed genes between enasidenib and DMSO treated CD71+ erythroid progenitors.

2019-11-08 | GSE140108 | GEO

Murine Bone Marrow Erythroid Cells Have Two Branches of Differentiation Defined by the Presence of CD45 and a Different Immune Transcriptome Than Fetal Liver Erythroid Cells

Project description:Ter-119 is a better murine erythroid selection marker than CD71 for bulk immunomics, murine bone marrow and fetal liver erythroid cells have different antimicrobial immune transcriptome signatures, murine bone marrow erythropoiesis is comprised of two branches In this study, we decided to benchmark erythroid cells’ selection and enrichment markers – CD71 and Ter-119 via bulk immune transcriptomics by Nanostring and perform bulk immune transcriptome profiling of Ter-119+ erythroid cells from the bone marrow and the fetal liver by Nanostring.

2023-07-31 | GSE238190 | GEO

CD71+ HSC/MPP

Project description:CD71+ HSC/MPP

| PRJNA789602 | ENA

scRNAseq of isolated fetal liver erythroid progenitor cell subpopulations, and CITE-seq of mouse fetal liver erythroid progenitors

Project description:We used scRNAseq to profile CD71/CD24low fetal liver erythroid progenitor cells isolated by 2 distinct methods: FACS and immunomagnetic isolation. Cells from both isolation methods were hashtagged using Biolegend mouse hashtag antibodies and library prepped together on the 10X chromium platform with the 3'RNA v3 kit. We also performed CITE-seq to profile proteogenomic expression of CD117 and CD71 on lineage-depleted mouse fetal liver erythroid progenitor cells. CITE-seq was performed through a separate library prep on the 10X chromium platform with the 3'RNAv3 kit.

2021-11-12 | GSE188287 | GEO

The immunoregulatory function of peripheral blood CD71<sup>+</sup> erythroid cells in systemic-onset juvenile idiopathic arthritis.

Project description:CD71+ erythroid cells (CECs) are recognized to have an immunoregulatory function via direct cell-cell interaction and soluble mediators. Circulating CECs appear in newborns or patients with hemolytic and cardiopulmonary disorders. To assess the biological role of CECs in systemic inflammation, we studied the gene expression and function in systemic-onset juvenile idiopathic arthritis (SoJIA). Peripheral blood mononuclear cells of SoJIA patients expressed upregulated erythropoiesis-related genes. It represented the largest expansion of CECs during active phase SoJIA among other inflammatory diseases. Despite the opposing roles of erythropoietin and hepcidin in erythropoiesis, both serum levels were in concert with the amounts of SoJIA-driven CECs. Circulating CECs counts in inflammatory diseases were positively correlated with the levels of C-reactive protein, IL-6, IL-18, or soluble TNF receptors. Co-culture with active SoJIA-driven CECs suppressed secretions of IL-1β, IL-6, and IL-8 from healthy donor monocytes. The top upregulated gene in SoJIA-driven CECs was ARG2 compared with CECs from cord blood controls, although cytokine production from monocytes was suppressed by co-culture, even with an arginase inhibitor. CECs are driven to the periphery during the acute phase of SoJIA at higher levels than other inflammatory diseases. Circulating CECs may control excessive inflammation via the immunoregulatory pathways, partly involving arginase-2.

| S-EPMC8277864 | biostudies-literature

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