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    New insights into the regulation of innate immunity by caspase-8

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    Author
    Sagulenko, V; Lawlor, KE; Vince, JE
    Date
    2016-01-13
    Source Title
    Arthritis Research and Therapy
    Publisher
    BIOMED CENTRAL LTD
    University of Melbourne Author/s
    Vince, James; Lawlor, Kathryn
    Affiliation
    Medical Biology (W.E.H.I.)
    Metadata
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    Document Type
    Journal Article
    Citations
    Sagulenko, V., Lawlor, K. E. & Vince, J. E. (2016). New insights into the regulation of innate immunity by caspase-8. ARTHRITIS RESEARCH & THERAPY, 18 (1), https://doi.org/10.1186/s13075-015-0910-0.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/258069
    DOI
    10.1186/s13075-015-0910-0
    Abstract
    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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