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Betsy J. Barnes

Researcher at Hofstra University

Publications -  10
Citations -  1331

Betsy J. Barnes is an academic researcher from Hofstra University. The author has contributed to research in topics: IRF5 & Immune system. The author has an hindex of 8, co-authored 10 publications receiving 744 citations. Previous affiliations of Betsy J. Barnes include The Feinstein Institute for Medical Research.

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Journal ArticleDOI

Neutrophil extracellular traps in COVID-19.

TL;DR: Sera from patients with COVID-19 have elevated levels of cell-free DNA, myeloperoxidase(MPO)-DNA, and citrullinated histone H3 (Cit-H3); the latter two are highly specific markers of NETs, which may contribute to cytokine release and respiratory failure.
Posted ContentDOI

Neutrophil extracellular traps (NETs) as markers of disease severity in COVID-19

TL;DR: Sera from patients with COVID-19 are reported to have elevated levels of cell-free DNA, myeloperoxidase(MPO)-DNA, and citrullinated histone H3 (Cit-H3); the latter two are highly specific markers of NETs, which may contribute to cytokine release and respiratory failure.
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Modulating Cytokine Production via Select Packaging and Secretion From Extracellular Vesicles.

TL;DR: This review will focus on these disease settings and summarize recent progress and mechanisms by which cytokines may be packaged within and modulated by EVs, as a therapeutic option for regulating innate and adaptive immunity.
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Inhibition of IRF5 hyperactivation protects from lupus onset and severity

TL;DR: This study provides the first in vivo clinical support for treating SLE patients with an IRF5 inhibitor and developed novel inhibitors that are cell permeable, non-toxic and selectively bind to the inactive IRf5 monomer.
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IRF5 genetic risk variants drive myeloid-specific IRF5 hyperactivation and presymptomatic SLE

TL;DR: Data support that individuals carrying the IRF5-SLE risk haplotype are more susceptible to environmental/stochastic influences that trigger chronic immune activation, predisposing to the development of clinical SLE.