We are analyzing https://link.springer.com/article/10.1186/s13075-015-0910-0.

Title:
New insights into the regulation of innate immunity by caspase-8 | Arthritis Research & Therapy
Description:
Caspase-8 is required for extrinsic apoptosis, but is also central for preventing a pro-inflammatory receptor interacting protein kinase (RIPK) 3–mixed lineage kinase domain-like (MLKL)-dependent cell death pathway termed necroptosis. Despite these critical cellular functions, the impact of capase-8 deletion in the myeloid cell lineage, which forms the basis for innate immune responses, has remained unclear. In a recent article in Arthritis Research & Therapy, Cuda et al. report that myeloid cell-restricted caspase-8 loss leads to a very mild RIPK3-dependent inflammatory phenotype. The presented results suggest that inflammation does not arise exclusively because of RIPK3-mediated necroptotic death but that, in the absence of caspase-8, RIPK1 and RIPK3 enhance microbiome-driven Toll-like receptor-induced pro-inflammatory cytokine production.
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Keywords {🔍}

caspase, ripk, article, pubmed, receptor, death, google, scholar, cell, cas, research, activation, responses, cells, kinase, necroptosis, deletion, cuda, cytokine, mice, tlr, inflammasome, apoptosis, myeloid, inflammatory, authors, central, immune, inflammation, production, ilβ, nlrp, arthritis, innate, lawlor, vince, protein, phenotype, mlkl, signalling, privacy, cookies, data, access, lineage, necroptotic, tolllike, macrophages, tnfr, roles,

Topics {✒️}

drive ripk3–mlkl-dependent necroptosis nf-kappab signaling lps-triggered il-1β activation necroptosis-induced cellular rupture ripk3 doubly-deficient mice casp8fl/fl lysmcre mice ripk3-mediated necroptotic death caspase-8-deficient myeloid cells strong pro-inflammatory phenotype cell-type specific deletion microbe-dependent tlr engagement article download pdf generate bioactive il-1β innate-immune cells increased splenic monocytes/macrophages activate pro-inflammatory interleukin innate immune responses abnormal immune responses pro-survival capacity myeloid cell lineage regulating immune responses lps-induced necroptosis reduced cytokine production casp8fl/fl lysmcre regulating cell death death receptor signalling adaptive immune responses adaptor protein fas privacy choices/manage cookies induce cytokine production achieve full activity il-1β production [11] induced lethality resulting arthritis res ther caspase-8 signalling downstream induce cell death reduced caspase-8 expression creative commons license inducing death receptor distinct transcriptional profile wild-type controls major inflammatory trigger activate ripk1/ripk3 pro-caspase-8 molecules direct caspase-8 proteolysis medical research council full access mice lacking caspase-8 downstream effector caspases precursor il-1β

Schema {🗺️}

WebPage:
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         headline:New insights into the regulation of innate immunity by caspase-8
         description:Caspase-8 is required for extrinsic apoptosis, but is also central for preventing a pro-inflammatory receptor interacting protein kinase (RIPK) 3–mixed lineage kinase domain-like (MLKL)-dependent cell death pathway termed necroptosis. Despite these critical cellular functions, the impact of capase-8 deletion in the myeloid cell lineage, which forms the basis for innate immune responses, has remained unclear. In a recent article in Arthritis Research & Therapy, Cuda et al. report that myeloid cell-restricted caspase-8 loss leads to a very mild RIPK3-dependent inflammatory phenotype. The presented results suggest that inflammation does not arise exclusively because of RIPK3-mediated necroptotic death but that, in the absence of caspase-8, RIPK1 and RIPK3 enhance microbiome-driven Toll-like receptor-induced pro-inflammatory cytokine production.
         datePublished:2016-01-13T00:00:00Z
         dateModified:2016-01-13T00:00:00Z
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      headline:New insights into the regulation of innate immunity by caspase-8
      description:Caspase-8 is required for extrinsic apoptosis, but is also central for preventing a pro-inflammatory receptor interacting protein kinase (RIPK) 3–mixed lineage kinase domain-like (MLKL)-dependent cell death pathway termed necroptosis. Despite these critical cellular functions, the impact of capase-8 deletion in the myeloid cell lineage, which forms the basis for innate immune responses, has remained unclear. In a recent article in Arthritis Research & Therapy, Cuda et al. report that myeloid cell-restricted caspase-8 loss leads to a very mild RIPK3-dependent inflammatory phenotype. The presented results suggest that inflammation does not arise exclusively because of RIPK3-mediated necroptotic death but that, in the absence of caspase-8, RIPK1 and RIPK3 enhance microbiome-driven Toll-like receptor-induced pro-inflammatory cytokine production.
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      dateModified:2016-01-13T00:00:00Z
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         Orthopedics
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                     name:Walter and Eliza Hall Institute, Parkville, Melbourne, Australia
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                  name:The University of Melbourne
                  address:
                     name:Department of Medical Biology, The University of Melbourne, Melbourne, Australia
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               name:Department of Medical Biology, The University of Melbourne, Melbourne, Australia
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            address:
               name:Walter and Eliza Hall Institute, Parkville, Melbourne, Australia
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      name:Walter and Eliza Hall Institute, Parkville, Melbourne, Australia
      name:Department of Medical Biology, The University of Melbourne, Melbourne, Australia
      name:Walter and Eliza Hall Institute, Parkville, Melbourne, Australia
      name:Department of Medical Biology, The University of Melbourne, Melbourne, Australia

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