Effect of nociceptive neuropeptides on dendritic cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE217502 | GEO | 2023/04/01
REPOSITORIES: GEO
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Project description:We explored the effects of nociceptors on DC under various conditions by means of in vitro coculture of Flt3L-induced bone marrow-derived DCs and primary mouse nociceptors.
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Project description:Multiple subsets of FLT3L-dependent dendritic cells (DCs) control T cell tolerance and immunity. In mouse tissues, CD8α-like DCs are identified by CD103 expression. This DC subset efficiently enters lymph nodes and cross-presents antigens, rendering CD103+ DCs promising targets for therapeutic tolerance induction or vaccination. However, only limited numbers of CD103+ DCs can be isolated with current methods. Moreover, bone marrow cultures with FLT3L produce complex mixtures of DC subsets. We developed a novel method for generating large numbers of Batf3-dependent CD103+ DCs. We used microarray analysis to compare in vitro generated CD103+ and CD103- DCs and correlated their expression patterns to published profiles and signatures of DC subsets.
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2011-06-22 | GSE29949 | GEO
Project description:The development of all dendritic cells (DCs) including antigen-presenting conventional DCs (cDCs) and cytokine-producing plasmacytoid DCs (pDCs) is controlled by the growth factor Flt3 ligand (Flt3L) and its receptor Flt3. We genetically dissected this common Flt3L-driven pathway of DCs differentiation using CRISPR/Cas9-based dropout screening in a Flt3L dependent progenitor cell line. Genome-wide screening identified multiple regulators of DC differentiation including the glycosylphosphatidylinositol transamidase complex and arginine methyltransferase Carm1, whose role was confirmed in vivo. It also showed that negative regulators of mTOR signaling, including the subunits of TSC and GATOR1 complexes, restricted progenitor growth but enabled DC differentiation, demonstrating that a TSC- and GATOR1-mediated shutdown of mTOR is required for the process. An orthogonal screen focused on transcriptional regulators showed that Trim33 (TIF-1g) is required for DC differentiation. Conditional targeting in vivo revealed an essential role of Trim33 in the development of all DCs, but not of monocytes or granulocytes. In particular, inducible deletion of Trim33 caused a rapid loss of all DC progenitors, pDCs and the cross-presenting cDC1 subset. The loss of Trim33 from DC progenitors caused spontaneous interferon and inflammatory response, aberrant induction of macrophage-specific genes, and failure to induce DC differentiation program. Collectively, these data elucidate common mechanisms that control Flt3L-driven differentiation of the entire DC lineage, and identify Trim33 as its essential regulator.
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Project description:To understand the functional relationship between brain dendritic cells (brain DCs) and other myeloid cells, we compared the gene expression profile of m/chDCs to that of bone marrow monocytes, brain microglia and classical spleen CD8+ and CD8- DCs. In order to obtain enough brain DCs for mRNA extraction, we expanded brain DCs with in vivo Flt3L treatment before purification. This study includes data from FACs Aria-purified brain DCs, bone marrow monocytes, brain microglia and classical spleen CD8+ and CD8- DCs. The genearray was performed to compare expression of cell surface endocytic receptor, cytokine receptors, TLRs, transcription factors, molecules for antigen processing and presentation. Each Series consists of 3 individuall samples
2011-06-22 | E-GEOD-29949 | biostudies-arrayexpress
Project description:The development of all dendritic cells (DCs) including antigen-presenting conventional DCs (cDCs) and cytokine-producing plasmacytoid DCs (pDCs) is controlled by the growth factor Flt3 ligand (Flt3L) and its receptor Flt3. We genetically dissected this common Flt3L-driven pathway of DCs differentiation using CRISPR/Cas9-based dropout screening in a Flt3L-dependent progenitor cell line. Genome-wide screening identified multiple regulators of DC differentiation including the glycosylphosphatidylinositol transamidase complex and arginine methyltransferase Carm1, whose role was confirmed in vivo. It also showed that negative regulators of mTOR signaling, including the subunits of TSC and GATOR1 complexes, restricted progenitor growth but enabled DC differentiation, demonstrating that a TSC- and GATOR1-mediated shutdown of mTOR is required for the process. An orthogonal screen focused on transcriptional regulators showed that Trim33 (TIF-1g) is required for DC differentiation. Conditional targeting in vivo revealed an essential role of Trim33 in the development of all DCs, but not of monocytes or granulocytes. In particular, inducible deletion of Trim33 caused a rapid loss of all DC progenitors, pDCs and the cross-presenting cDC1 subset. The loss of Trim33 from DC progenitors caused spontaneous interferon and inflammatory response, aberrant induction of macrophage-specific genes, and failure to induce DC differentiation program. Collectively, these data elucidate common mechanisms that control Flt3L-driven differentiation of the entire DC lineage, and identify Trim33 as its essential regulator.
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Project description:The development of all dendritic cells (DCs) including antigen-presenting conventional DCs (cDCs) and cytokine-producing plasmacytoid DCs (pDCs) is controlled by the growth factor Flt3 ligand (Flt3L) and its receptor Flt3. We genetically dissected this common Flt3L-driven pathway of DCs differentiation using CRISPR/Cas9-based dropout screening in a Flt3L-dependent progenitor cell line. Genome-wide screening identified multiple regulators of DC differentiation including the glycosylphosphatidylinositol transamidase complex and arginine methyltransferase Carm1, whose role was confirmed in vivo. It also showed that negative regulators of mTOR signaling, including the subunits of TSC and GATOR1 complexes, restricted progenitor growth but enabled DC differentiation, demonstrating that a TSC- and GATOR1-mediated shutdown of mTOR is required for the process. An orthogonal screen focused on transcriptional regulators showed that Trim33 (TIF-1g) is required for DC differentiation. Conditional targeting in vivo revealed an essential role of Trim33 in the development of all DCs, but not of monocytes or granulocytes. In particular, inducible deletion of Trim33 caused a rapid loss of all DC progenitors, pDCs and the cross-presenting cDC1 subset. The loss of Trim33 from DC progenitors caused spontaneous interferon and inflammatory response, aberrant induction of macrophage-specific genes, and failure to induce DC differentiation program. Collectively, these data elucidate common mechanisms that control Flt3L-driven differentiation of the entire DC lineage, and identify Trim33 as its essential regulator.
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Project description:The development of all dendritic cells (DCs) including antigen-presenting conventional DCs (cDCs) and cytokine-producing plasmacytoid DCs (pDCs) is controlled by the growth factor Flt3 ligand (Flt3L) and its receptor Flt3. We genetically dissected this common Flt3L-driven pathway of DCs differentiation using CRISPR/Cas9-based dropout screening in a Flt3L dependent progenitor cell line. Genome-wide screening identified multiple regulators of DC differentiation including the glycosylphosphatidylinositol transamidase complex and arginine methyltransferase Carm1, whose role was confirmed in vivo. It also showed that negative regulators of mTOR signaling, including the subunits of TSC and GATOR1 complexes, restricted progenitor growth but enabled DC differentiation, demonstrating that a TSC- and GATOR1-mediated shutdown of mTOR is required for the process. An orthogonal screen focused on transcriptional regulators showed that Trim33 (TIF-1g) is required for DC differentiation. Conditional targeting in vivo revealed an essential role of Trim33 in the development of all DCs, but not of monocytes or granulocytes. In particular, inducible deletion of Trim33 caused a rapid loss of all DC progenitors, pDCs and the cross-presenting cDC1 subset. The loss of Trim33 from DC progenitors caused spontaneous interferon and inflammatory response, aberrant induction of macrophage-specific genes, and failure to induce DC differentiation program. Collectively, these data elucidate common mechanisms that control Flt3L-driven differentiation of the entire DC lineage, and identify Trim33 as its essential regulator.
2024-04-12 | GSE259391 | GEO
Project description:The development of all dendritic cells (DCs) including antigen-presenting conventional DCs (cDCs) and cytokine-producing plasmacytoid DCs (pDCs) is controlled by the growth factor Flt3 ligand (Flt3L) and its receptor Flt3. We genetically dissected this common Flt3L-driven pathway of DCs differentiation using CRISPR/Cas9-based dropout screening in a Flt3L-dependent progenitor cell line. Genome-wide screening identified multiple regulators of DC differentiation including the glycosylphosphatidylinositol transamidase complex and arginine methyltransferase Carm1, whose role was confirmed in vivo. It also showed that negative regulators of mTOR signaling, including the subunits of TSC and GATOR1 complexes, restricted progenitor growth but enabled DC differentiation, demonstrating that a TSC- and GATOR1-mediated shutdown of mTOR is required for the process. An orthogonal screen focused on transcriptional regulators showed that Trim33 (TIF-1g) is required for DC differentiation. Conditional targeting in vivo revealed an essential role of Trim33 in the development of all DCs, but not of monocytes or granulocytes. In particular, inducible deletion of Trim33 caused a rapid loss of all DC progenitors, pDCs and the cross-presenting cDC1 subset. The loss of Trim33 from DC progenitors caused spontaneous interferon and inflammatory response, aberrant induction of macrophage-specific genes, and failure to induce DC differentiation program. Collectively, these data elucidate common mechanisms that control Flt3L-driven differentiation of the entire DC lineage, and identify Trim33 as its essential regulator.
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Project description:Few families of signaling factors have been implicated in the control of development. Here we identify the neuropeptides nociceptin and somatostatin, a neurotransmitter and neuroendocrine hormone, as a class of developmental signals in chick and zebrafish. We show that signals from the anterior mesendoderm are required for the formation of anterior placode progenitors with one of the signals being somatostatin. Somatostatin controls ectodermal expression of nociceptin and both peptides regulate Pax6 in lens and olfactory progenitors. Consequently, loss of somatostatin and nociceptin signaling leads to severe reduction of lens formation. Our findings not only uncover these neuropeptides as developmental signals, but also identify a long-sought-after mechanism that initiates Pax6 in placode progenitors and may explain the ancient evolutionary origin of neuropeptides, pre-dating a complex nervous system. We used progenitors for anterior and posterior sensory placodes dissected from chick embryos HH5-7; these were either processed immediately or cultured for 5 hrs to hybridise to Affymetrix chick array. We aimed to identify genes that are co regualted with Pax6, a key regulator of lens and olfactory progenitor cells. Pax6 is normally present in anterior, but not posterior placode precursors, but upregulated in both after 5 hrs culture.
2014-04-25 | E-GEOD-48116 | biostudies-arrayexpress