Caspase-11 Mediated Cell Death Contributes to the Pathogenesis of Imiquimod-Induced Psoriasis
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2019Access:
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Sin?ad Kenealy∗, Joan Manils∗, Mathilde Raverdeau Natalia Munoz-Wolf, Gillian Barber, Alex Liddicoat, Ed C.Lavelle Emma M.Creagh, Caspase-11 Mediated Cell Death Contributes to the Pathogenesis of Imiquimod-Induced Psoriasis, Journal of Investigative Dermatology, 2019, 2389 - 2393Abstract:
Inflammasomes are multiprotein complexes that respond to infection or injury to activate inflammation. Inflammatory caspases, caspase-1, 4 and 5 in humans, and their murine orthologues caspase-1 and 11 are crucial components of inflammasomes, responsible for the maturation and secretion of IL-1β and IL-18, and for pyroptosis (inflammatory cell death) (Creagh, 2014). Psoriasis is a chronic inflammatory skin condition with a range of clinical manifestations. The most common manifestation is chronic plaque psoriasis, where the adaptive immune response predominates. However innate and autoinflammatory events, governed by IL-1β (Martinez-Quiles and Goldbach-Mansky, 2018), prevail in pustular forms of psoriasis (Liang et al., 2017).
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PUBLISHEDDOI: 10.1016/j.jid.2019.05.010
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Journal of Investigative DermatologyAvailability:
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Caspase-1 and -11 (casp1/11), Imiquimod (IMQ), Double knockout (DKO), Terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL), Lipopolysaccharide (LPS), Lactate dehydrogenase (LDH), Bone marrow derived macrophage (BMDM)DOI:
https://doi.org/10.1016/j.jid.2019.05.010Metadata
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