SARS-CoV-2 spike protein interacts with and activates TLR41
By A Mystery Man Writer
Description
SARS-CoV-2 spike and nucleocapsid proteins fail to activate human dendritic cells or γδ T cells
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SARS-CoV-2 activates the TLR4/MyD88 pathway in human macrophages: A possible correlation with strong pro-inflammatory responses in severe COVID-19 - ScienceDirect
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SARS-CoV-2 Omicron Spike shows strong binding affinity and favourable interaction landscape with the TLR4/MD2 compared to other variants - ScienceDirect
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Exploring the immunogenic properties of SARS-CoV-2 structural proteins: PAMP:TLR signaling in the mediation of the neuroinflammatory and neurologic sequelae of COVID-19 - ScienceDirect
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Interferon antagonists encoded by SARS-CoV-2 at a glance
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IJMS, Free Full-Text
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SARS-CoV-2 Spike protein is not pro-inflammatory in human primary macrophages: endotoxin contamination and lack of protein glycosylation as possible confounders
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SARS-CoV-2 nucleocapsid protein, rather than spike protein, triggers a cytokine storm originating from lung epithelial cells in patients with COVID-19
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SARS-CoV-2 spike protein induces a differential monocyte activation that may contribute to age bias in COVID-19 severity
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SARS-CoV-2 spike protein induces the cytokine release syndrome by stimulating T cells to produce more IL-2
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Frontiers Early suppression of antiviral host response and protocadherins by SARS-CoV-2 Spike protein in THP-1-derived macrophage-like cells
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SARS-CoV-2 spike protein induces the cytokine release syndrome by stimulating T cells to produce more IL-2
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