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Charles A. Dinarello

Researcher at University of Colorado Denver

Publications -  1073
Citations -  152254

Charles A. Dinarello is an academic researcher from University of Colorado Denver. The author has contributed to research in topics: Interleukin & Cytokine. The author has an hindex of 190, co-authored 1058 publications receiving 139668 citations. Previous affiliations of Charles A. Dinarello include University of Guadalajara & Pennsylvania State University.

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Toll-like receptors and chronic inflammation in rheumatic diseases: new developments

TL;DR: Novel insights on the role of TLRs in several inflammatory joint diseases, including rheumatoid arthritis, systemic lupus erythematosus, gout and Lyme arthritis are reviewed, with a focus on the signalling mechanisms mediated by the Toll–IL-1 receptor (TIR) domain.
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Thrombin induces endothelial type II activation in vitro: IL-1 and TNF-alpha-independent IL-8 secretion and E-selectin expression.

TL;DR: It is demonstrated that in addition to short term endothelial activation, thrombin also functions as a long acting proinflammatory agent by inducing endothelial synthesis of the mediators required for neutrophils activation and extravazation during inflammation.
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Intrinsic Pituitary Interleukin-1β Is Induced by Bacterial Lipopolysaccharide*

TL;DR: The marked increase in anterior pituitary IL- 1β message after the administration of bacterial lipopolysaccharide, raises the possibility that IL-1β may be involved in paracrine or autocrine regulation of pituitaries function during infectious challenge.
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Modulation of cell proliferation and cytokine production in acute myeloblastic leukemia by interleukin-1 receptor antagonist and lack of its expression by leukemic cells

TL;DR: Data show a role for IL-1 in the spontaneous proliferation and cytokine production of AML cells and suggest that an imbalanced synthesis ofIL-1 and of its natural receptor antagonist may contribute to the unrestricted growth ofAML cells.
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Histone deacetylase inhibitors prevent exocytosis of interleukin-1β-containing secretory lysosomes: role of microtubules

TL;DR: Observations indicate that a functional microtubule network is required for IL-1beta secretion and suggest that disruption of tubulin is the mechanism by which inhibitors of HDACs reduce the secretion of IL- 1beta.