Kevin J. Tracey
The Feinstein Institute for Medical Research
609 Papers
4.5K Citations
Kevin J. Tracey is an academic researcher from The Feinstein Institute for Medical Research. The author has contributed to research in topics: Inflammation & Medicine. The author has an hindex of 138, co-authored 561 publications. Previous affiliations of Kevin J. Tracey include Memorial Sloan Kettering Cancer Center & Hofstra University.
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Papers
High Mobility Group Box Protein 1: An Endogenous Signal for Dendritic Cell Maturation and Th1 Polarization
Davorka Messmer,Huan Yang,Huan Yang,Gloria Telusma,Faye Knoll,Jianhua Li,Jianhua Li,Bradley T. Messmer,Kevin J. Tracey,Kevin J. Tracey,Nicholas Chiorazzi +10 more
TL;DR: It is shown that HMGB1, via its B box domain, induced phenotypic maturation of DCs, as evidenced by increased CD83, CD54, CD80, CD40, CD58, and MHC class II expression and decreased CD206 expression.
Brain acetylcholinesterase activity controls systemic cytokine levels through the cholinergic anti-inflammatory pathway.
Valentin A. Pavlov,William R. Parrish,Mauricio Rosas-Ballina,Mahendar Ochani,Margot Gallowitsch Puerta,Kanta Ochani,Sangeeta S. Chavan,Yousef Al-Abed,Kevin J. Tracey +8 more
TL;DR: Findings show that inhibition of brain acetylcholinesterase suppresses systemic inflammation through a central muscarinic receptor-mediated and vagal- and alpha7nAChR-dependent mechanism, and indicate that a clinically used centrally-acting acetylCholinestersterase inhibitor can be utilized to suppress abnormal inflammation to therapeutic advantage.
Redox modification of cysteine residues regulates the cytokine activity of high mobility group box-1 (HMGB1).
Huan Yang,Peter Lundbäck,Lars Ottosson,Helena Erlandsson-Harris,Emilie Venereau,Marco Bianchi,Yousef Al-Abed,Ulf Andersson,Kevin J. Tracey,Daniel J. Antoine +9 more
TL;DR: It is established that the C106 thiol and the C23-C45 disulfide bond are required for HMGB1 to induce nuclear NF-κB translocation and tumor necrosis factor (TNF) production in macrophages.
Neural regulation of immunity: molecular mechanisms and clinical translation
TL;DR: Findings from recent clinical studies of bioelectronic neuromodulation in inflammatory and autoimmune diseases are summarized and mechanistic insights are outlined focusing on translational relevance and conceptual developments.
431
The HMGB1 Receptor RAGE Mediates Ischemic Brain Damage
Sajjad Muhammad,Waleed Barakat,S. B. Stoyanov,Sasidhar Murikinati,Huan Yang,Kevin J. Tracey,Martin Bendszus,Grazisa Rossetti,Peter P. Nawroth,Angelika Bierhaus,Markus Schwaninger +10 more
TL;DR: Evidence is provided that the receptor for advanced glycation end products (RAGE) functions as a sensor of necrotic cell death and contributes to inflammation and ischemic brain damage in stroke and HMGB1–RAGE signaling may provide a target for anti-inflammatory therapy in stroke.
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