The Experts below are selected from a list of 109272 Experts worldwide ranked by ideXlab platform
Michelle Makiya - One of the best experts on this subject based on the ideXlab platform.
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the long non coding rna morrbid regulates bim and short lived Myeloid Cell lifespan
Nature, 2016Co-Authors: Jonathan J Kotzin, Sean P Spencer, Sam J Mccright, Dinesh Babu Uthaya Kumar, Magalie A Collet, Walter K Mowel, Ellen N Elliott, Asli Uyar, Michelle MakiyaAbstract:The long non-coding RNA Morrbid controls Myeloid Cell lifespan and regulates apoptosis by repressing the adjacent pro-apoptotic Bcl2l11 gene in cis. Neutrophils, eosinophils and 'classical' monocytes are a first line of defense against pathogens, but their actions can also cause inflammatory diseases. It is important that the lifespan of these Myeloid Cells is regulated in order to minimize deleterious effects. Jorge Henao-Mejia and colleagues show here that a long non-coding RNA termed Morrbid specifically controls the lifespan of short-lived Myeloid Cells by regulating expression of the pro-apoptotic Bcl2l11 (Bim) gene. MORRBID is present in humans and is highly upregulated in human hypereosinophilic diseases, so its inhibition may represent a novel therapeutic approach in pathologies influenced by altered Myeloid lifespan. Neutrophils, eosinophils and ‘classical’ monocytes collectively account for about 70% of human blood leukocytes and are among the shortest-lived Cells in the body1,2. Precise regulation of the lifespan of these Myeloid Cells is critical to maintain protective immune responses and minimize the deleterious consequences of prolonged inflammation1,2. However, how the lifespan of these Cells is strictly controlled remains largely unknown. Here we identify a long non-coding RNA that we termed Morrbid, which tightly controls the survival of neutrophils, eosinophils and classical monocytes in response to pro-survival cytokines in mice. To control the lifespan of these Cells, Morrbid regulates the transcription of the neighbouring pro-apoptotic gene, Bcl2l11 (also known as Bim), by promoting the enrichment of the PRC2 complex at the Bcl2l11 promoter to maintain this gene in a poised state. Notably, Morrbid regulates this process in cis, enabling allele-specific control of Bcl2l11 transcription. Thus, in these highly inflammatory Cells, changes in Morrbid levels provide a locus-specific regulatory mechanism that allows rapid control of apoptosis in response to extraCellular pro-survival signals. As MORRBID is present in humans and dysregulated in individuals with hypereosinophilic syndrome, this long non-coding RNA may represent a potential therapeutic target for inflammatory disorders characterized by aberrant short-lived Myeloid Cell lifespan.
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the long non coding rna morrbid regulates bim and short lived Myeloid Cell lifespan
Nature, 2016Co-Authors: Jonathan J Kotzin, Sean P Spencer, Sam J Mccright, Dinesh Babu Uthaya Kumar, Magalie A Collet, Walter K Mowel, Ellen N Elliott, Asli Uyar, Michelle MakiyaAbstract:Neutrophils, eosinophils and 'classical' monocytes collectively account for about 70% of human blood leukocytes and are among the shortest-lived Cells in the body. Precise regulation of the lifespan of these Myeloid Cells is critical to maintain protective immune responses and minimize the deleterious consequences of prolonged inflammation. However, how the lifespan of these Cells is strictly controlled remains largely unknown. Here we identify a long non-coding RNA that we termed Morrbid, which tightly controls the survival of neutrophils, eosinophils and classical monocytes in response to pro-survival cytokines in mice. To control the lifespan of these Cells, Morrbid regulates the transcription of the neighbouring pro-apoptotic gene, Bcl2l11 (also known as Bim), by promoting the enrichment of the PRC2 complex at the Bcl2l11 promoter to maintain this gene in a poised state. Notably, Morrbid regulates this process in cis, enabling allele-specific control of Bcl2l11 transcription. Thus, in these highly inflammatory Cells, changes in Morrbid levels provide a locus-specific regulatory mechanism that allows rapid control of apoptosis in response to extraCellular pro-survival signals. As MORRBID is present in humans and dysregulated in individuals with hypereosinophilic syndrome, this long non-coding RNA may represent a potential therapeutic target for inflammatory disorders characterized by aberrant short-lived Myeloid Cell lifespan.
Sean P Spencer - One of the best experts on this subject based on the ideXlab platform.
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the long non coding rna morrbid regulates bim and short lived Myeloid Cell lifespan
Nature, 2016Co-Authors: Jonathan J Kotzin, Sean P Spencer, Sam J Mccright, Dinesh Babu Uthaya Kumar, Magalie A Collet, Walter K Mowel, Ellen N Elliott, Asli Uyar, Michelle MakiyaAbstract:The long non-coding RNA Morrbid controls Myeloid Cell lifespan and regulates apoptosis by repressing the adjacent pro-apoptotic Bcl2l11 gene in cis. Neutrophils, eosinophils and 'classical' monocytes are a first line of defense against pathogens, but their actions can also cause inflammatory diseases. It is important that the lifespan of these Myeloid Cells is regulated in order to minimize deleterious effects. Jorge Henao-Mejia and colleagues show here that a long non-coding RNA termed Morrbid specifically controls the lifespan of short-lived Myeloid Cells by regulating expression of the pro-apoptotic Bcl2l11 (Bim) gene. MORRBID is present in humans and is highly upregulated in human hypereosinophilic diseases, so its inhibition may represent a novel therapeutic approach in pathologies influenced by altered Myeloid lifespan. Neutrophils, eosinophils and ‘classical’ monocytes collectively account for about 70% of human blood leukocytes and are among the shortest-lived Cells in the body1,2. Precise regulation of the lifespan of these Myeloid Cells is critical to maintain protective immune responses and minimize the deleterious consequences of prolonged inflammation1,2. However, how the lifespan of these Cells is strictly controlled remains largely unknown. Here we identify a long non-coding RNA that we termed Morrbid, which tightly controls the survival of neutrophils, eosinophils and classical monocytes in response to pro-survival cytokines in mice. To control the lifespan of these Cells, Morrbid regulates the transcription of the neighbouring pro-apoptotic gene, Bcl2l11 (also known as Bim), by promoting the enrichment of the PRC2 complex at the Bcl2l11 promoter to maintain this gene in a poised state. Notably, Morrbid regulates this process in cis, enabling allele-specific control of Bcl2l11 transcription. Thus, in these highly inflammatory Cells, changes in Morrbid levels provide a locus-specific regulatory mechanism that allows rapid control of apoptosis in response to extraCellular pro-survival signals. As MORRBID is present in humans and dysregulated in individuals with hypereosinophilic syndrome, this long non-coding RNA may represent a potential therapeutic target for inflammatory disorders characterized by aberrant short-lived Myeloid Cell lifespan.
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the long non coding rna morrbid regulates bim and short lived Myeloid Cell lifespan
Nature, 2016Co-Authors: Jonathan J Kotzin, Sean P Spencer, Sam J Mccright, Dinesh Babu Uthaya Kumar, Magalie A Collet, Walter K Mowel, Ellen N Elliott, Asli Uyar, Michelle MakiyaAbstract:Neutrophils, eosinophils and 'classical' monocytes collectively account for about 70% of human blood leukocytes and are among the shortest-lived Cells in the body. Precise regulation of the lifespan of these Myeloid Cells is critical to maintain protective immune responses and minimize the deleterious consequences of prolonged inflammation. However, how the lifespan of these Cells is strictly controlled remains largely unknown. Here we identify a long non-coding RNA that we termed Morrbid, which tightly controls the survival of neutrophils, eosinophils and classical monocytes in response to pro-survival cytokines in mice. To control the lifespan of these Cells, Morrbid regulates the transcription of the neighbouring pro-apoptotic gene, Bcl2l11 (also known as Bim), by promoting the enrichment of the PRC2 complex at the Bcl2l11 promoter to maintain this gene in a poised state. Notably, Morrbid regulates this process in cis, enabling allele-specific control of Bcl2l11 transcription. Thus, in these highly inflammatory Cells, changes in Morrbid levels provide a locus-specific regulatory mechanism that allows rapid control of apoptosis in response to extraCellular pro-survival signals. As MORRBID is present in humans and dysregulated in individuals with hypereosinophilic syndrome, this long non-coding RNA may represent a potential therapeutic target for inflammatory disorders characterized by aberrant short-lived Myeloid Cell lifespan.
Jonathan J Kotzin - One of the best experts on this subject based on the ideXlab platform.
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the long non coding rna morrbid regulates bim and short lived Myeloid Cell lifespan
Nature, 2016Co-Authors: Jonathan J Kotzin, Sean P Spencer, Sam J Mccright, Dinesh Babu Uthaya Kumar, Magalie A Collet, Walter K Mowel, Ellen N Elliott, Asli Uyar, Michelle MakiyaAbstract:The long non-coding RNA Morrbid controls Myeloid Cell lifespan and regulates apoptosis by repressing the adjacent pro-apoptotic Bcl2l11 gene in cis. Neutrophils, eosinophils and 'classical' monocytes are a first line of defense against pathogens, but their actions can also cause inflammatory diseases. It is important that the lifespan of these Myeloid Cells is regulated in order to minimize deleterious effects. Jorge Henao-Mejia and colleagues show here that a long non-coding RNA termed Morrbid specifically controls the lifespan of short-lived Myeloid Cells by regulating expression of the pro-apoptotic Bcl2l11 (Bim) gene. MORRBID is present in humans and is highly upregulated in human hypereosinophilic diseases, so its inhibition may represent a novel therapeutic approach in pathologies influenced by altered Myeloid lifespan. Neutrophils, eosinophils and ‘classical’ monocytes collectively account for about 70% of human blood leukocytes and are among the shortest-lived Cells in the body1,2. Precise regulation of the lifespan of these Myeloid Cells is critical to maintain protective immune responses and minimize the deleterious consequences of prolonged inflammation1,2. However, how the lifespan of these Cells is strictly controlled remains largely unknown. Here we identify a long non-coding RNA that we termed Morrbid, which tightly controls the survival of neutrophils, eosinophils and classical monocytes in response to pro-survival cytokines in mice. To control the lifespan of these Cells, Morrbid regulates the transcription of the neighbouring pro-apoptotic gene, Bcl2l11 (also known as Bim), by promoting the enrichment of the PRC2 complex at the Bcl2l11 promoter to maintain this gene in a poised state. Notably, Morrbid regulates this process in cis, enabling allele-specific control of Bcl2l11 transcription. Thus, in these highly inflammatory Cells, changes in Morrbid levels provide a locus-specific regulatory mechanism that allows rapid control of apoptosis in response to extraCellular pro-survival signals. As MORRBID is present in humans and dysregulated in individuals with hypereosinophilic syndrome, this long non-coding RNA may represent a potential therapeutic target for inflammatory disorders characterized by aberrant short-lived Myeloid Cell lifespan.
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the long non coding rna morrbid regulates bim and short lived Myeloid Cell lifespan
Nature, 2016Co-Authors: Jonathan J Kotzin, Sean P Spencer, Sam J Mccright, Dinesh Babu Uthaya Kumar, Magalie A Collet, Walter K Mowel, Ellen N Elliott, Asli Uyar, Michelle MakiyaAbstract:Neutrophils, eosinophils and 'classical' monocytes collectively account for about 70% of human blood leukocytes and are among the shortest-lived Cells in the body. Precise regulation of the lifespan of these Myeloid Cells is critical to maintain protective immune responses and minimize the deleterious consequences of prolonged inflammation. However, how the lifespan of these Cells is strictly controlled remains largely unknown. Here we identify a long non-coding RNA that we termed Morrbid, which tightly controls the survival of neutrophils, eosinophils and classical monocytes in response to pro-survival cytokines in mice. To control the lifespan of these Cells, Morrbid regulates the transcription of the neighbouring pro-apoptotic gene, Bcl2l11 (also known as Bim), by promoting the enrichment of the PRC2 complex at the Bcl2l11 promoter to maintain this gene in a poised state. Notably, Morrbid regulates this process in cis, enabling allele-specific control of Bcl2l11 transcription. Thus, in these highly inflammatory Cells, changes in Morrbid levels provide a locus-specific regulatory mechanism that allows rapid control of apoptosis in response to extraCellular pro-survival signals. As MORRBID is present in humans and dysregulated in individuals with hypereosinophilic syndrome, this long non-coding RNA may represent a potential therapeutic target for inflammatory disorders characterized by aberrant short-lived Myeloid Cell lifespan.
Falko Steinbach - One of the best experts on this subject based on the ideXlab platform.
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characterization of the Myeloid Cell populations resident in the porcine palatine tonsil
Frontiers in Immunology, 2018Co-Authors: Ferran Soldevila, Jane C Edwards, Simon P Graham, Lisa M Stevens, Bentley Crudgington, Helen R Crooke, Dirk Werling, Falko SteinbachAbstract:The palatine tonsil is the portal of entry for food and air, and is continuously subjected to environmental challenges including pathogens which use the tonsil and pharynx as a primary site of replication. In pigs, this includes the viruses causing porcine respiratory and reproductive syndrome, and classical and African swine fever; diseases which have impacted the pig production industry globally. Despite the importance of tonsils in host defence, little is known regarding the phenotype of the Myeloid Cells resident in the porcine tonsil. Here, we have characterised five Myeloid Cell populations that align to orthologous populations defined in other mammalian species: a CD4+ plasmacytoid DC (pDC) defined by expression of the conserved markers E2.2 and IRF-7, a conventional dendritic Cell (cDC1) population expressing CADM1highCD172alow and high levels of XCR1 able to activate allogeneic CD4 and CD8 T Cells; a cDC2 population of CADM1dim Cells expressing FLT3, IRF4 and CSF1R with an ability to activate allogeneic CD4 T Cells; CD163+ macrophages (MƟs) defined by high levels of endocytosis and responsiveness to LPS and finally a CD14+ population likely derived from a myelo-monocytic lineage, which showed the highest levels of endocytosis, a capacity for activation of CD4+ memory Cells, combined with lower relative expression of FLT3. Increased knowledge regarding the phenotypic and functional properties of Myeloid Cells resident in porcine tonsil, will enable these Cells to be targeted for future vaccination strategies to current and emerging porcine viruses.
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Characterization of the Myeloid Cell Populations’ Resident in the Porcine Palatine Tonsil
Frontiers Media S.A., 2018Co-Authors: Ferran Soldevila, Jane C Edwards, Simon P Graham, Lisa M Stevens, Bentley Crudgington, Helen R Crooke, Dirk Werling, Falko SteinbachAbstract:The palatine tonsil is the portal of entry for food and air and is continuously subjected to environmental challenges, including pathogens, which use the tonsil and pharynx as a primary site of replication. In pigs, this includes the viruses causing porcine respiratory and reproductive syndrome, and classical and African swine fever; diseases that have impacted the pig production industry globally. Despite the importance of tonsils in host defense, little is known regarding the phenotype of the Myeloid Cells resident in the porcine tonsil. Here, we have characterized five Myeloid Cell populations that align to orthologous populations defined in other mammalian species: a CD4+ plasmacytoid dendritic Cell (DC) defined by expression of the conserved markers E2.2 and IRF-7, a conventional dendritic Cell (cDC1) population expressing CADM1highCD172alow and high levels of XCR1 able to activate allogeneic CD4 and CD8 T Cells; a cDC2 population of CADM1dim Cells expressing FLT3, IRF4, and CSF1R with an ability to activate allogeneic CD4 T Cells; CD163+ macrophages (Mϴs) defined by high levels of endocytosis and responsiveness to LPS and finally a CD14+ population likely derived from the myelomonocytic lineage, which showed the highest levels of endocytosis, a capacity for activation of CD4+ memory T Cells, combined with lower relative expression of FLT3. Increased knowledge regarding the phenotypic and functional properties of Myeloid Cells resident in porcine tonsil will enable these Cells to be targeted for future vaccination strategies to current and emerging porcine viruses
Sam J Mccright - One of the best experts on this subject based on the ideXlab platform.
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the long non coding rna morrbid regulates bim and short lived Myeloid Cell lifespan
Nature, 2016Co-Authors: Jonathan J Kotzin, Sean P Spencer, Sam J Mccright, Dinesh Babu Uthaya Kumar, Magalie A Collet, Walter K Mowel, Ellen N Elliott, Asli Uyar, Michelle MakiyaAbstract:The long non-coding RNA Morrbid controls Myeloid Cell lifespan and regulates apoptosis by repressing the adjacent pro-apoptotic Bcl2l11 gene in cis. Neutrophils, eosinophils and 'classical' monocytes are a first line of defense against pathogens, but their actions can also cause inflammatory diseases. It is important that the lifespan of these Myeloid Cells is regulated in order to minimize deleterious effects. Jorge Henao-Mejia and colleagues show here that a long non-coding RNA termed Morrbid specifically controls the lifespan of short-lived Myeloid Cells by regulating expression of the pro-apoptotic Bcl2l11 (Bim) gene. MORRBID is present in humans and is highly upregulated in human hypereosinophilic diseases, so its inhibition may represent a novel therapeutic approach in pathologies influenced by altered Myeloid lifespan. Neutrophils, eosinophils and ‘classical’ monocytes collectively account for about 70% of human blood leukocytes and are among the shortest-lived Cells in the body1,2. Precise regulation of the lifespan of these Myeloid Cells is critical to maintain protective immune responses and minimize the deleterious consequences of prolonged inflammation1,2. However, how the lifespan of these Cells is strictly controlled remains largely unknown. Here we identify a long non-coding RNA that we termed Morrbid, which tightly controls the survival of neutrophils, eosinophils and classical monocytes in response to pro-survival cytokines in mice. To control the lifespan of these Cells, Morrbid regulates the transcription of the neighbouring pro-apoptotic gene, Bcl2l11 (also known as Bim), by promoting the enrichment of the PRC2 complex at the Bcl2l11 promoter to maintain this gene in a poised state. Notably, Morrbid regulates this process in cis, enabling allele-specific control of Bcl2l11 transcription. Thus, in these highly inflammatory Cells, changes in Morrbid levels provide a locus-specific regulatory mechanism that allows rapid control of apoptosis in response to extraCellular pro-survival signals. As MORRBID is present in humans and dysregulated in individuals with hypereosinophilic syndrome, this long non-coding RNA may represent a potential therapeutic target for inflammatory disorders characterized by aberrant short-lived Myeloid Cell lifespan.
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the long non coding rna morrbid regulates bim and short lived Myeloid Cell lifespan
Nature, 2016Co-Authors: Jonathan J Kotzin, Sean P Spencer, Sam J Mccright, Dinesh Babu Uthaya Kumar, Magalie A Collet, Walter K Mowel, Ellen N Elliott, Asli Uyar, Michelle MakiyaAbstract:Neutrophils, eosinophils and 'classical' monocytes collectively account for about 70% of human blood leukocytes and are among the shortest-lived Cells in the body. Precise regulation of the lifespan of these Myeloid Cells is critical to maintain protective immune responses and minimize the deleterious consequences of prolonged inflammation. However, how the lifespan of these Cells is strictly controlled remains largely unknown. Here we identify a long non-coding RNA that we termed Morrbid, which tightly controls the survival of neutrophils, eosinophils and classical monocytes in response to pro-survival cytokines in mice. To control the lifespan of these Cells, Morrbid regulates the transcription of the neighbouring pro-apoptotic gene, Bcl2l11 (also known as Bim), by promoting the enrichment of the PRC2 complex at the Bcl2l11 promoter to maintain this gene in a poised state. Notably, Morrbid regulates this process in cis, enabling allele-specific control of Bcl2l11 transcription. Thus, in these highly inflammatory Cells, changes in Morrbid levels provide a locus-specific regulatory mechanism that allows rapid control of apoptosis in response to extraCellular pro-survival signals. As MORRBID is present in humans and dysregulated in individuals with hypereosinophilic syndrome, this long non-coding RNA may represent a potential therapeutic target for inflammatory disorders characterized by aberrant short-lived Myeloid Cell lifespan.
