C
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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Interleukin 1 induces a shock-like state in rabbits. Synergism with tumor necrosis factor and the effect of cyclooxygenase inhibition.
TL;DR: IL-1, like TNF, possesses the ability to induce hemodynamic and hematological changes typical of septic shock, and that the combination of IL-1 and TNF is more potent than either agent alone.
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Cytokine-induced expression of HIV-1 in a chronically infected promonocyte cell line.
TL;DR: A model system for cytokine-induced up-regulation of human immunodeficiency virus type 1 (HIV-1) expression in chronically infected promonocyte clones was established and can be used to delineate the potential mechanisms whereby HIV-1 infection regulates cellular gene expression.
Journal Article
Interleukin-1 induces a shock-like state in rabbits: synergism with tumor necrosis factor and the effect of cyclooxygenase inhibition.
TL;DR: In addition to activating T and B lymphocytes, interleukin-1 (IL-1) induces several hematologic and metabolic changes typical of host responses to infection and injury.
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Interleukin-6 (IL-6) as an anti-inflammatory cytokine: induction of circulating IL-1 receptor antagonist and soluble tumor necrosis factor receptor p55
TL;DR: The results suggest that the antinflammatory properties of IL-6 may be due; in part, to the induction ofIL-1Ra synthesis and the release of soluble TNF receptors, and suggest that tissue macrophages may be an important source of Il-6-induced IL-1 Ra.
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Anti-inflammatory Agents: Present and Future
TL;DR: The new era of anti-inflammatory agents includes "biologicals" such as anticytokine therapies and small molecules that block the activity of kinases and small RNAs.