Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1016/S2665-9913(20)30340-4 http://scihub22266oqcxt.onion/10.1016/S2665-9913(20)30340-4 33073244!7546716!33073244     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Lancet+Rheumatol 2020 ; 2 (12): e779-e790 Nephropedia Template TP {{tp|p=33073244|t=2020. Imperfect storm: is interleukin-33 the Achilles heel of COVID-19?|pdf=|usr=}}{{33073244}} gab.com Text Imperfect storm: is interleukin-33 the Achilles heel of COVID-19 JO: Lancet Rheumatol http://www.kidney.de/pget.php?&tw=1&pmid=33073244 #FOAvip The unique cytokine signature of COVID-19 might provide clues to disease mechanisms and possible future therapies. Here, we propose a pathogenic model in which the alarmin cytokine, interleukin (IL)-33, is a key player in driving all stages of COVID-19 disease (ie, asymptomatic, mild-moderate, severe-critical, and chronic-fibrotic). In susceptible individuals, IL-33 release by damaged lower respiratory cells might induce dysregulated GATA-binding factor 3-expressing regulatory T cells, thereby breaking immune tolerance and eliciting severe acute respiratory syndrome coronavirus 2-induced autoinflammatory lung disease. Such disease might be initially sustained by IL-33-differentiated type-2 innate lymphoid cells and locally expanded gammadelta T cells. In severe COVID-19 cases, the IL-33-ST2 axis might act to expand the number of pathogenic granulocyte-macrophage colony-stimulating factor-expressing T cells, dampen antiviral interferon responses, elicit hyperinflammation, and favour thromboses. In patients who survive severe COVID-19, IL-33 might drive pulmonary fibrosis by inducing myofibroblasts and epithelial-mesenchymal transition. We discuss the therapeutic implications of these hypothetical pathways, including use of therapies that target IL-33 (eg, anti-ST2), T helper 17-like gammadelta T cells, immune cell homing, and cytokine balance. Twit Text FOAVip Imperfect storm: is interleukin-33 the Achilles heel of COVID-19 ????Lancet Rheumatol http://www.kidney.de/pget.php?&tw=1&pmid=33073244 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33073244 #FOAvip English Wikipedia <ref>{{Cite pmid|33073244}}</ref> Imperfect storm: is interleukin-33 the Achilles heel of COVID-19? #MMPMID33073244 Zizzo G; Cohen PL Lancet Rheumatol 2020[Dec]; 2 (12): e779-e790 PMID33073244show ga The unique cytokine signature of COVID-19 might provide clues to disease mechanisms and possible future therapies. Here, we propose a pathogenic model in which the alarmin cytokine, interleukin (IL)-33, is a key player in driving all stages of COVID-19 disease (ie, asymptomatic, mild-moderate, severe-critical, and chronic-fibrotic). In susceptible individuals, IL-33 release by damaged lower respiratory cells might induce dysregulated GATA-binding factor 3-expressing regulatory T cells, thereby breaking immune tolerance and eliciting severe acute respiratory syndrome coronavirus 2-induced autoinflammatory lung disease. Such disease might be initially sustained by IL-33-differentiated type-2 innate lymphoid cells and locally expanded gammadelta T cells. In severe COVID-19 cases, the IL-33-ST2 axis might act to expand the number of pathogenic granulocyte-macrophage colony-stimulating factor-expressing T cells, dampen antiviral interferon responses, elicit hyperinflammation, and favour thromboses. In patients who survive severe COVID-19, IL-33 might drive pulmonary fibrosis by inducing myofibroblasts and epithelial-mesenchymal transition. We discuss the therapeutic implications of these hypothetical pathways, including use of therapies that target IL-33 (eg, anti-ST2), T helper 17-like gammadelta T cells, immune cell homing, and cytokine balance. äImperfect storm: is interleukin-33 the Achilles heel of COVID-19?(epmc).pdf DeepDyve Pubget Overpricing