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Open AccessJournal ArticleDOI

Cytokine Storm.

David C. Fajgenbaum, +1 more
- 03 Dec 2020 - 
- Vol. 383, Iss: 23, pp 2255-2273
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TLDR
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.

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References
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Impaired natural killer activity in lymphohistiocytosis syndrome

TL;DR: The findings indicate that testing NK activity is useful for the diagnosis of lymphohistiocytosis syndrome and can be used as an index of activity of the disease, among other major clinical and biologic signs of this syndrome.
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Hyperinduction of Cyclooxygenase-2-Mediated Proinflammatory Cascade: A Mechanism for the Pathogenesis of Avian Influenza H5N1 Infection

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Protection against lethal bacterial infection in mice by monocyte-chemotactic and -activating factor.

TL;DR: In vivo effect on the survival of mice paralleled the reduced recovery of viable P. aeruginosa or S. typhimurium from the peritoneal cavity, since MCAF exhibited chemotaxis on murine macrophages as well as enhanced phagocytosis and killing of bacteria in vitro, is responsible for eliminating bacteria and thus enhancing the survival rate.
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The Mechanism of Superantigen-Mediated Toxic Shock: Not a Simple Th1 Cytokine Storm

TL;DR: The results demonstrate unequivocally that TCRαβ T cells are critical for lethality in toxic shock but it is the early TNF-α response and not the later cytokine surge that mediates lethal shock.
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Preclinical In Vivo Modeling of Cytokine Release Syndrome Induced by ErbB-Retargeted Human T Cells: Identifying a Window of Therapeutic Opportunity?

TL;DR: These data demonstrate that CAR-induced cytokine release syndrome can be modeled in mice that express target Ag in an appropriate distribution, and argue that ErbB-retargeted T cells can achieve therapeutic benefit in the absence of unacceptable toxicity, providing that route of administration and dose are carefully optimized.
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