Cytokine Storm.
David C. Fajgenbaum,Carl H. June +1 more
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From the Department of Medicine, Division of Translational Medicine and Human Genetics, Center for Cytokine Storm Treatment and Laboratory, and the Center for Cellular Immunotherapies and the Parker Institute for Cancer Immunotherapy, University of Pennsylvania, Philadelphia.Abstract:
From the Department of Medicine, Division of Translational Medicine and Human Genetics, Center for Cytokine Storm Treatment and Laboratory (D.C.F.), and the Center for Cellular Immunotherapies and the Parker Institute for Cancer Immunotherapy (C.H.J.), Perelman School of Medicine, University of Pennsylvania, Philadelphia. Address reprint requests to Dr. Fajgenbaum at davidfa@ pennmedicine . upenn . edu or to Dr. June at cjune@ upenn . edu.read more
Citations
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Interleukin-6 Receptor Antagonists in Critically Ill Patients with Covid-19.
TL;DR: In this paper, the authors evaluated tocilizumab and sarilumab in an ongoing international, multifactorial, adaptive platform trial, which used a Bayesian statistical model with predefined criteria for superiority, efficacy, equivalence or futility.
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Endothelial dysfunction and immunothrombosis as key pathogenic mechanisms in COVID-19.
Aldo Bonaventura,Aldo Bonaventura,Alessandra Vecchié,Lorenzo Dagna,Kimberly Martinod,Dave L. Dixon,Benjamin W. Van Tassell,Francesco Dentali,Fabrizio Montecucco,Steffen Massberg,Marcel Levi,Antonio Abbate +11 more
TL;DR: In this paper, the authors proposed that SARS-CoV-2 infection induces a process known as immunothrombosis, in which activated neutrophils and monocytes interact with platelets and the coagulation cascade, leading to intravascular clot formation in small and larger vessels.
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COVID-19 and the human innate immune system.
TL;DR: In this article, a conceptual framework for the interaction of the human innate immune system with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was provided to link the clinical observations with experimental findings that have been made during the first year of the pandemic.
Journal ArticleDOI
Tofacitinib in Patients Hospitalized with Covid-19 Pneumonia.
Patrícia O. Guimarães,Daniel Quirk,Remo H. Furtado,Lilia N. Maia,José F. Saraiva,Murillo Oliveira Antunes,Roberto Kalil Filho,Vagner Madrini Junior,Alexandre de Matos Soeiro,Alexandre P. Tognon,Viviane C Veiga,Priscilla de Aquino Martins,Diogo D.F. Moia,Bruna S. Sampaio,Silvia R.L. Assis,Ronaldo V P Soares,Luciana P.A. Piano,Kleber Castilho,Roberta G.R.A.P. Momesso,Frederico Monfardini,Hélio Penna Guimarães,Dario Ponce de Leon,Majori Dulcine,Marcia Pinheiro,Levent M. Gunay,J. Jasper Deuring,Luiz Vicente Rizzo,Tamas Koncz,Otavio Berwanger +28 more
TL;DR: Among patients hospitalized with Covid-19 pneumonia, tofacitinib led to a lower risk of death or respiratory failure through day 28 than placebo, and the proportional odds of having a worse score on the eight-level ordinal scale with tofacinib, as compared with placebo.
Journal ArticleDOI
The signal pathways and treatment of cytokine storm in COVID-19.
TL;DR: In this paper, the authors discuss the latest developments in the immunopathological characteristics of COVID-19 and focus on CS including the current research status of the different cytokines involved, and discuss the induction, function, downstream signaling and existing and potential interventions for targeting these cytokines or related signal pathways.
References
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IL-12 Deaths: Explanation and a Puzzle
TL;DR: Researchers investigating toxic reactions that killed two patients in a trial of interleukin-12 earlier this year have reached a surprising conclusion: the drug is highly toxic if it is given in multiple high doses, but those effects can be avoided if the multiple doses are preceded by a single dose followed by a rest period.
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Repeated TLR9 stimulation results in macrophage activation syndrome–like disease in mice
Edward M. Behrens,Scott W. Canna,Katharine Slade,Sheila Rao,Portia A. Kreiger,Michele Paessler,Taku Kambayashi,Gary A. Koretzky +7 more
TL;DR: It is shown that repeated stimulation of TLR9 produced an HLH/MAS-like syndrome on a normal genetic background, without exogenous antigen, and that IL-10 played a protective role in this model and that blocking IL- 10 signaling led to the development of hemophagocytosis.
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