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
The Effects of Selective Hematopoietic Expression of Human IL-37 on Systemic Inflammation and Atherosclerosis in LDLr-Deficient Mice.
Geerte Hoeke,P. Padmini S.J. Khedoe,Janna A. van Diepen,Karin Pike-Overzet,Britt Van de Ven,Nadia Vazirpanah,Isabel M. Mol,Pieter S. Hiemstra,Frank J. T. Staal,Rinke Stienstra,Mihai G. Netea,Charles A. Dinarello,Patrick C.N. Rensen,Jimmy F.P. Berbée +13 more
TL;DR: It is concluded that under low-grade inflammatory conditions, hematopoietic IL-37 expression reduces the inflammatory state, but does not influence atherosclerosis development in hyperlipidemic LDLr-deficient mice.
Book ChapterDOI
Biological consequences of monocyte activation during hemodialysis.
Journal ArticleDOI
T cell–mediated hepatic inflammation modulates adiponectin levels in mice: role of tumor necrosis factor α
Alison M. Morris,Joseph A. Sennello,Raja Fayad,Robert H. Eckel,Charles A. Dinarello,Giamila Fantuzzi +5 more
TL;DR: It is shown that inflammation-induced TNF-α is a critical mediator of adipose-tissue-derived adiponectin in vivo and this was associated with restored circulating levels of adiponECTin.
Journal ArticleDOI
Hyperosmolar sodium chloride, p38 mitogen activated protein and cytokine-mediated inflammation.
TL;DR: The link between inflammation and salt intake likely includes p38 MAPK as hyperosmolar sodium chloride triggers phosphorylation of p38MAPK and stimulates gene expression and synthesis of proinflammatory cytokines.
Journal ArticleDOI
Inflammation in rheumatology in 2015: New tools to tackle inflammatory arthritis.
TL;DR: A targetable mechanism of uric-acid-induced inflammation in gouty arthritis and the expected efficacy — but unforeseen safety concerns — of anti-IL-17 antibodies are highlighted.