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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.

Papers
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Journal ArticleDOI

Recombinant Human Alpha-1 Antitrypsin-Fc Fusion Protein Reduces Mouse Myocardial Inflammatory Injury After Ischemia-Reperfusion Independent of Elastase Inhibition.

TL;DR: The pAAT and recombinant human AAT-Fc reduce the acute myocardial inflammatory injury after ischemia–reperfusion in the mouse leading to preservation of viable myocardium and systolic function, independent on the effects on neutrophil elastase.
Patent

Inhibitors of serine protease activity and their use in methods and compositions for treatment of graft rejection and promotion of graft survival

TL;DR: In this paper, the authors present methods of treating and preventing transplantation and side effects associated with transplantation, in particular, compositions and methods for inhibition of graft rejection and promotion of graft survival.
Journal ArticleDOI

IL-1 family cytokines as drivers and inhibitors of trained immunity

TL;DR: In this article, the role of anti-inflammatory members of the IL-1 family of cytokines (IL-1F) which interfere with the inflammatory process has been discussed, with the potential to regulate the induction of a trained phenotype.
Journal ArticleDOI

Comparison of First Use and Reuse of Cuprophan Membranes on Interleukin-1 Receptor Antagonist and Interleukin-1β Production by Blood Mononuclear Cells

TL;DR: This work studied the hemodialysis-induced changes in the in vitro production of interleukin-1 receptor antagonist (IL-1Ra) and IL-1 beta by peripheral blood mononuclear cells (PBMCs), and compared the effect of first use and reuse of cuprophan membranes on these changes.
Journal Article

Elevated circulating levels of soluble interleukin-1 receptor type II during interleukin-2 immunotherapy.

TL;DR: IL-1sRII, unlike IL-1Ra, remains a modest, natural, anti-inflammatory mechanism triggered by immunotherapy withIL-2, but not with IL-6, the results indicate.