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ATAC-seq and mRNA-seq of the following human primary CD4 T cell subsets: GM-CSF producing, GM-CSF negative, bulk, memory and naive CD4 T cells.

ABSTRACT: ATAC-seq and mRNA-seq of the following human primary CD4 T cell subsets: GM-CSF producing, GM-CSF negative, bulk, memory and naive CD4 T cells.

PROVIDER: PRJNA490149 | ENA |

REPOSITORIES: ENA

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mRNA-seq of the following human primary CD4 T cell subsets: GM-CSF producing, GM-CSF negative, bulk, memory and naive CD4 T cells.

Project description:mRNA-seq of the following human primary CD4 T cell subsets: GM-CSF producing, GM-CSF negative, bulk, memory and naive CD4 T cells.

| PRJNA490153 | ENA

ATAC-seq of the following human primary CD4 T cell subsets: GM-CSF producing, GM-CSF negative, bulk, memory and naive CD4 T cells.

Project description:ATAC-seq of the following human primary CD4 T cell subsets: GM-CSF producing, GM-CSF negative, bulk, memory and naive CD4 T cells.

| PRJNA490154 | ENA

mRNA-seq of the following human primary CD4 T cell subsets: GM-CSF producing, GM-CSF negative, bulk, memory and naive CD4 T cells.

Project description:Above primary T cell subsets were isolated by magnetic isolation (including GM-CSF capture and secretion assay) from peripheral blood of 5 to 6 human healthy donors. Total RNA (and genomic DNA for an accompanying dataset) was extracted for transcriptome analysis. By integration of RNA-seq data with corresponding ATAC-seq data we generated a novel gene regulatory network of human GM-CSF producing and memory T helper cells.

2021-07-21 | GSE119732 | GEO

ATAC-seq of the following human primary CD4 T cell subsets: GM-CSF producing, GM-CSF negative, bulk, memory and naive CD4 T cells.

Project description:Above primary T cell subsets were isolated by magnetic isolation (including GM-CSF capture and secretion assay) from peripheral blood of 5 to 6 human healthy donors. Genomic DNA (and total RNA for an accompanying dataset) was extracted and processed for ATAC-seq to determine DNA accessibility. By integration of ATAC-seq data with corresponding RNA-seq data we generated a novel gene regulatory network of human GM-CSF producing and memory T helper cells.

2021-07-21 | GSE119731 | GEO

Single cell immune profiling reveals a developmentally distinct CD4+ GM-CSF+ T cell lineage that induces GI tract GVHD

Project description:Gastrointestinal (GI) tract involvement is a major determinant for subsequent morbidity and mortality arising during graft versus host disease (GVHD). CD4+ T cells that produce GM-CSF have emerged as central mediators of inflammation in this tissue site as GM-CSF serves as a critical cytokine link between the adaptive and innate arms of the immune system. However, cellular heterogeneity within the CD4+ GM-CSF+ T cell population due to the concurrent production of other inflammatory cytokines has raised questions as to whether these cells have a common ontology or if there exists a unique CD4+ GM-CSF+ subset that differs from other defined T helper (TH) subtypes. Using single cell RNA sequencing analysis, we identified two CD4+ GM-CSF+ T cell populations that arose during GVHD and were distinguishable by the presence or absence of IFN-γ co-expression. CD4+ GM-CSF+ IFN-γ- T cells which emerged preferentially in the colon had a distinct transcriptional profile, employed unique gene regulatory networks, and possessed a non-overlapping TCR repertoire when compared to CD4+ GM-CSF+ IFN-γ+ T cells as well as all other transcriptionally defined CD4+ T cell populations in the colon. Functionally, this CD4+ GM-CSF+ T cell population contributed to pathological damage in the GI tract which was critically dependent upon signaling through the IL-7 receptor but was independent of type 1 interferon signaling. Thus, these studies help to unravel heterogeneity within CD4+ GM-CSF+ T cells that arise during GVHD and define a developmentally distinct colitogenic TH GM-CSF+ subset that mediates immunopathology.

2022-01-14 | GSE193475 | GEO

miRNA expression microarrays in GM-CSF or GM-CSF+IL6-induced mouse MDSC

Project description:Myeloid-derived suppressor cells (MDSCs) have emerged as major regulators of immune responses in cancer and other pathological conditions. Multiple factors including cytokines, transcription factors and multiple signaling pathways are involved in MDSC differentiation. Cytokines such as granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin(IL-6) etc could in vitro mediate development of MDSCs.IL-6 with GM-CSF mediated MDSC not only had stronger suppressive function but also the dynamics of their suppressive function was different from GM-CSF alone mediated MDSCs.To found a new regulatory factor (s) in tumor and inflammatory environments, we compared GM-CSF and IL-6 mediated MDSCs with GM-CSF alone mediated MDSCs using lncRNA microarray, miRNA microarrays and protein-coding mRNA microarrays.

2017-10-09 | GSE104719 | GEO

Loss of GM-CSF-dependent instruction of alveolar macrophages in COVID-19 provides a rationale for inhaled GM-CSF treatment (RNA-Seq)

Project description:Systemic GM-CSF promotes myelopoiesis and inflammation and GM-CSF blockade is being evaluated as treatment for COVID-19-associated hyperinflammation. Alveolar GM-CSF is however required for monocytes to differentiate into alveolar macrophages (AM) that control alveolar homeostasis and dampen inflammation. By mapping cross-species AM development stages to clinical lung samples, we discovered that COVID-19 is marked by defective GM-CSF-dependent AM instruction and accumulation of proinflammatory macrophages. In a multi-center, open-label, randomized, controlled trial in 81 non-ventilated COVID-19 patients with respiratory failure, we found that inhalation of rhu-GM-CSF did not improve mean oxygenation parameters compared with standard treatment. However, more patients on GM-CSF had a clinical response, and GM-CSF inhalation induced higher numbers of virus-specific CD8 effector lymphocytes and class-switched B cells, without exacerbating systemic hyperinflammation. This translational proof-of-concept study provides rationale for further testing of inhaled GM-CSF as non-invasive treatment to improve alveolar gas exchange and simultaneously boost anti-viral immunity in COVID-19

2022-11-03 | GSE216704 | GEO

mRNA and long noncoding RNA expression microarrays in GM-CSF or GM-CSF+IL6-induced mouse MDSC

2017-10-09 | GSE104718 | GEO

GM-CSF induced gene-regulation in human monocytes

Project description:Human and murine studies showed that granulocyte macrophage colony-stimulating factor (GM-CSF) exerts beneficial effects in intestinal inflammation. To explore whether GM-CSF mediates its effects via monocytes, we analyzed effects of GM-CSF on monocytes in vitro and assessed the immunomodulatory potential of GM-CSF-activated monocytes (GMaM). We used microarray technology and functional assays to characterize GMaM in vitro and used a mouse model of colitis to study GMaM functions in vivo.

2014-11-27 | GSE63662 | GEO

NK cell-derived GM-CSF is critical for enhancing pathological arthritis

Project description:GM-CSF is involved in immune complex (IC)-mediated arthritis. However, little is known about what is the cellular source of GM-CSF and how it is regulated during IC-mediated inflammation. Using novel GM-CSF reporter mice, we show that NK cells produce GM-CSF during an IC-mediated model of inflammatory arthritis. NK cells promoted STIA in a GM-CSF-dependent manner, as deletion of NK cells and selective removal of GM-CSF production by NK cells abrogated disease. Furthermore, we show that myeloid cell activation by GM-CSF is restrained by induction of JAK/STAT checkpoint inhibitor cytokine-inducible SH2-containing protein, CIS. Myeloid cells from CIS-deficient mice had exaggerated responses to GM-CSF, and these mice develop exacerbated STIA. Our data suggest that tissue NK cells may amplify joint inflammation in arthritis via GM-CSF production and thus represent a novel target in IC-mediated pathology. Endogenous CIS provides a key brake on signaling through the GM-CSF receptor and strategies that boost its function may provide an alternative anti-inflammatory approach.

2020-02-19 | PXD012794 | Pride

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