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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004302naa a2200385 4500
001oai:DiVA.org:liu-174353
003SwePub
008210320s2021 | |||||||||||000 ||eng|
024a https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-1743532 URI
024a https://doi.org/10.1016/j.jid.2020.07.0122 DOI
040 a (SwePub)liu
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Verma, Deepti,d 1969-u Linköpings universitet,Avdelningen för cellbiologi,Medicinska fakulteten,Ingrid Asp Psoriasis Research Centre4 aut0 (Swepub:liu)deeve22
2451 0a Enhanced Inflammasome Activity in Patients with Psoriasis Promotes Systemic Inflammation
264 1b Elsevier,c 2021
338 a electronic2 rdacarrier
500 a Funding agencies: Ingrid Asp Foundation, the Edvard Welander Foundation, the Swedish Psoriasis Association, and the Medical Research Council of Southeast Sweden.
520 a Psoriasis is linked to systemic inflammation and cardiovascular comorbidities, but studies of the underlying cellular mechanisms are lacking. The NLRP3 inflammasome is genetically associated with psoriasis, and its activation is increasingly linked with cardiovascular disease. In this study, we show that patients with psoriasis exhibited higher plasma levels of inflammasome-generated IL-1ß and IL-18, without any correlation to skin lesion severity. Increased constitutive expression of the inflammasome sensors NLRP3, NLRP1, and AIM2 was found in peripheral blood cells of the patients and also of those with mild disease, and this was accompanied by an increased caspase-1 reactivity in the myeloid blood subsets. TNF-a was found to activate selectively the NLRP3 inflammasome without the requirement for a priming signal. TNF-a was found to signal through the TNFR?caspase-8?caspase-1 alternative inflammasome pathway, which proceeds independently of pyroptosis. Patients who received anti-TNF therapy had normalized plasma IL-1ß and IL-18 levels as well as normalized caspase-1 reactivity. This was in contrast to the patients treated with methotrexate who exhibited persistent, increased caspase-1 reactivity. Thus, we show that the TNF-a-mediated activation of NLRP3 inflammasomes in patients with psoriasis may contribute to systemic inflammation. Anti-TNF therapy normalized inflammasome function, suggesting a mechanism for the cardiovascular risk?reducing effect.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Reumatologi och inflammation0 (SwePub)302102 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Rheumatology and Autoimmunity0 (SwePub)302102 hsv//eng
700a Zamani Fekri, Shorau Linköpings universitet,Avdelningen för cellbiologi,Medicinska fakulteten,Ingrid Asp Psoriasis Research Centre4 aut0 (Swepub:liu)shoza26
700a Sigurdardottir, Gunnthorunn,d 1975-u Linköpings universitet,Avdelningen för cellbiologi,Medicinska fakulteten,Region Östergötland, Hudkliniken i Östergötland,Ingrid Asp Psoriasis Research Centre4 aut0 (Swepub:liu)gunsi16
700a Bivik, Cecilia,d 1978-u Linköpings universitet,Avdelningen för cellbiologi,Medicinska fakulteten,Ingrid Asp Psoriasis Research Centre4 aut0 (Swepub:liu)cecbi55
700a Sandin, Charlotta,d 1976-u Linköpings universitet,Avdelningen för cellbiologi,Medicinska fakulteten,Ingrid Asp Psoriasis Research Centre4 aut0 (Swepub:liu)chasa61
700a Enerbäck, Charlotta,d 1965-u Linköpings universitet,Avdelningen för cellbiologi,Medicinska fakulteten,Region Östergötland, Hudkliniken i Östergötland,Ingrid Asp Psoriasis Research Centre4 aut0 (Swepub:liu)chaen00
710a Linköpings universitetb Avdelningen för cellbiologi4 org
773t Journal of Investigative Dermatologyd : Elsevierg 141:3, s. 586-595.e5q 141:3<586-595.e5x 0022-202Xx 1523-1747
856u https://doi.org/10.1016/j.jid.2020.07.012y Fulltext
856u https://liu.diva-portal.org/smash/get/diva2:1538667/FULLTEXT01.pdfx primaryx Raw objecty fulltext:print
856u http://www.jidonline.org/article/S0022202X20319436/pdf
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-174353
8564 8u https://doi.org/10.1016/j.jid.2020.07.012

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