scispace - formally typeset
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.

Papers
More filters
Journal ArticleDOI

Isolation of an interleukin-1-like factor from human joint effusions.

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.
Journal ArticleDOI

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.
Journal ArticleDOI

IL-1α and IL-1β Recruit Different Myeloid Cells and Promote Different Stages of Sterile Inflammation

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.
Journal ArticleDOI

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.