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James R. Springstead

Researcher at Western Michigan University

Publications -  20
Citations -  1104

James R. Springstead is an academic researcher from Western Michigan University. The author has contributed to research in topics: Endothelial stem cell & Compressed sensing. The author has an hindex of 11, co-authored 19 publications receiving 829 citations. Previous affiliations of James R. Springstead include University of California, Los Angeles & University of Western Ontario.

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An endogenous caspase-11 ligand elicits interleukin-1 release from living dendritic cells

TL;DR: It is reported that encounters with microbial products and self-encoded oxidized phospholipids (oxPAPC) induce an enhanced DC activation state, which is called “hyperactive” and induce potent adaptive immune responses and are elicited by caspase-11, an enzyme that binds oxP APC and bacterial lipopolysaccharide (LPS).
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Role of Phospholipid Oxidation Products in Atherosclerosis

TL;DR: This review focuses on the mechanisms by which Ox-PL interact with endothelial cells, monocyte/macrophages, platelets, smooth muscle cells, and HDL to promote atherogenesis.
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By Capturing Inflammatory Lipids Released from Dying Cells, the Receptor CD14 Induces Inflammasome-Dependent Phagocyte Hyperactivation

TL;DR: It is found that the bacterial lipopolysaccharide receptor CD14 captured extracellular oxPAPC and delivered these lipids into the cell to promote inflammasome‐dependent DC hyperactivation, and it is reported that CD14 captures distinct lipids within oxP APC to promote dendritic cell and/or macrophage hyperactivation.
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Endogenous oxidized phospholipids reprogram cellular metabolism and boost hyperinflammation.

TL;DR: It is demonstrated that oxPAPC generates a distinctive metabolic and hyperinflammatory profile in macrophages that can drive atherosclerosis in mice, thereby underscoring the importance of DAMP-mediated activities in pathophysiological conditions.