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Richard J. Ulevitch

Researcher at Scripps Research Institute

Publications -  240
Citations -  50508

Richard J. Ulevitch is an academic researcher from Scripps Research Institute. The author has contributed to research in topics: Innate immune system & CD14. The author has an hindex of 102, co-authored 239 publications receiving 49181 citations. Previous affiliations of Richard J. Ulevitch include French Institute of Health and Medical Research & University of Pennsylvania.

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Book ChapterDOI

Recognition of bacterial endotoxins by receptor-dependent mechanisms.

TL;DR: The LBP/CD14-dependent pathway of cell stimulation has been identified and has particular importance for LPS recognition and signaling by cells such as monocytes/macrophages or polymorphonuclear leukocytes that constitutively express CD14.
Journal ArticleDOI

Antibodies against CD14 protect primates from endotoxin-induced shock.

TL;DR: Inhibition of the CD14 pathway represents a novel therapeutic approach to treating this life-threatening condition and is demonstrated for the first time in a primate model that is similar to human septic shock.
Journal ArticleDOI

Murine CD14 gene expression in vivo: extramyeloid synthesis and regulation by lipopolysaccharide.

TL;DR: It is demonstrated that CD14 gene expression is not restricted to myeloid cells, and that the level of expression of CD14 is influenced by exposure to LPS.
Journal ArticleDOI

Structure-activity relationship of synthetic toll-like receptor 4 agonists.

TL;DR: A novel set of synthetic lipid A mimetic compounds known as aminoalkyl glucosaminide phosphates, assessed via the induction of chemokines and cytokines following in vivo administration, demonstrate a clear dependence of length on secondary acyl chain on Toll-like receptor 4 activation.
Journal ArticleDOI

A critical role for monocytes and CD14 in endotoxin-induced endothelial cell activation.

TL;DR: Data suggest that the indirect pathway of LPS activation of endothelial cell is mediated by monocytes and mCD14 through the secretion of a soluble mediator(s), far more efficient than the direct, plasma-dependent pathway.