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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Journal ArticleDOI
Isolation of an interleukin-1-like factor from human joint effusions.
David D. Wood,Earl J. Ihrie,Charles A. Dinarello,Charles A. Dinarello,Philip L. Cohen,Philip L. Cohen +5 more
TL;DR: Joint fluids from patients with serveral different arthritides tested suggest that IL-1 is present in joint effusions and, therefore, might contribute to joint destruction.
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A specific receptor antagonist for interleukin 1 prevents Escherichia coli-induced shock in rabbits.
TL;DR: It is concluded that specific blockade of IL 1 at the receptor level demonstrates an essential role for this cytokine in the pathogenesis of septic shock.
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IL-1α and IL-1β Recruit Different Myeloid Cells and Promote Different Stages of Sterile Inflammation
Peleg Rider,Yaron Carmi,Ofer Guttman,Alex Braiman,Idan Cohen,Elena Voronov,Malka R. White,Charles A. Dinarello,Ron N. Apte +8 more
TL;DR: IL-1α, released from dying cells, initiates sterile inflammation by inducing recruitment of neutrophils, whereas IL-1β promotes the recruitment and retention of macrophages, which suggest new insight into the biology of IL- 1 molecules as well as on the regulation of sterile inflammation.
Journal Article
Prostaglandins posttranscriptionally inhibit monocyte expression of interleukin 1 activity by increasing intracellular cyclic adenosine monophosphate.
TL;DR: The data suggest that prostaglandins participate in an autoregulatory pathway that posttranscriptionally reduces expression of IL 1 activity, and this effect was reversed by indomethacin.
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Treating inflammation by blocking interleukin-1 in humans.
TL;DR: By specifically blocking IL-1, a great deal is learned about the role of this cytokine in inflammation but equally important, reducingIL-1 activity has lifted the burden of disease for many patients.