Prof. Diego Centonze
1. Department of Systems Medicine, Tor Vergata University, Rome, 00133, Italy 2. Unit of Neurology, IRCCS Neuromed, 86077 Pozzilli (IS), Italy
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Academic Career Length
31Years (1996-Present)
(Calculated once Scilit publication data is synced: current year − year of first publication + 1)
Representative Publications
View All Publications15 August 2007 in Blood
Journal Article
GBGiovanna Borsellino
Giovanna BorsellinoMKMarkus KLEINEWIETFELD
Markus KLEINEWIETFELDDMDiletta Di Mitri
Diletta Di MitriASAlexander Sternjak
Alexander Sternjak
ADAdamo Diamantini
Adamo Diamantini
KFKirsten Falk
Kirsten Falk
+8
In the immune system, extracellular ATP functions as a “natural adjuvant” that exhibits multiple proinflammatory effects. It is released by damaged cells as an indicator of trauma and cell death but can be inactivated by CD39 (nucleoside triphosphate diphosphohydrolase-1 [NTPDase 1]), an ectoenzyme that degrades ATP to AMP. Here, we show that CD39 is expressed primarily by immune-suppressive Foxp3+ regulatory T (Treg) cells. In mice, the enzyme is present on virtually all CD4+CD25+ cells. CD39 expression is driven by the Treg-specific transcription factor Foxp3 and its catalytic activity is strongly enhanced by T-cell receptor (TCR) ligation. Activated Treg cells are therefore able to abrogate ATP-related effects such as P2 receptor-mediated cell toxicity and ATP-driven maturation of dendritic cells. Also, human Treg cells express CD39. In contrast to mice, CD39 expression in man is restricted to a subset of Foxp3+ regulatory effector/memory-like T (TREM) cells. Notably, patients with the remitting/relapsing form of multiple sclerosis (MS) have strikingly reduced numbers of CD39+ Treg cells in the blood. Thus, in humans CD39 is a marker of a Treg subset likely involved in the control of the inflammatory autoimmune disease.
1 March 2018 in The Lancet
Journal Article
LKLudwig Kappos
Ludwig KapposABAmit Bar-Or
Amit Bar-Or
BCBruce A C Cree
Bruce A C CreeRFRobert J Fox
Robert J Fox
GGGavin Giovannoni
Gavin Giovannoni
Tjalf Ziemssen +321
31 March 2003 in Nature Neuroscience
Journal Article
Barbara PicconiDiego CentonzeKHKerstin Håkansson
Kerstin Håkansson
GBGiorgio Bernardi
Giorgio Bernardi
PGPaul Greengard
Paul Greengard
PCPaolo Calabresi
Paolo Calabresi
+2
1 March 2000 in Trends in Neurosciences
Journal Article
PCPaolo Calabresi
Paolo Calabresi
Diego CentonzePGPaolo Gubellini
Paolo Gubellini
Antonio PisaniGBGiorgio Bernardi
Giorgio Bernardi
18 March 2009 in Journal of Neuroscience
Journal Article
Diego CentonzeLMLuca Muzio
Luca MuzioSRSilvia Rossi
Silvia RossiFCFrancesca Cavasinni
Francesca Cavasinni
VCValentina De Chiara
Valentina De Chiara
GMGianvito Martino
Gianvito Martino +14
Neurodegeneration is the irremediable pathological event occurring during chronic inflammatory diseases of the CNS. Here we show that, in experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis, inflammation is capable in enhancing glutamate transmission in the striatum and in promoting synaptic degeneration and dendritic spine loss. These alterations occur early in the disease course, are independent of demyelination, and are strongly associated with massive release of tumor necrosis factor-α from activated microglia. CNS invasion by myelin-specific blood-borne immune cells is the triggering event, and the downregulation of the early geneArc/Arg3.1, leading to the abnormal expression and phosphorylation of AMPA receptors, represents a culminating step in this cascade of neurodegenerative events. Accordingly, EAE-induced synaptopathy subsided during pharmacological blockade of AMPA receptors. Our data establish a link between neuroinflammation and synaptic degeneration and calls for early neuroprotective therapies in chronic inflammatory diseases of the CNS.
1 March 2001 in European Journal of Neuroscience
Journal Article
Diego CentonzeBarbara PicconiPGPaolo Gubellini
Paolo Gubellini
GBGiorgio Bernardi
Giorgio Bernardi
PCPaolo Calabresi
Paolo CalabresiAbout Me
Diego Centonze is a full professor of Neurology at the Department of Systems Medicine of the University of Rome Tor Vergata and the director of the Neurology Unit and of the Neurorehabilitation Unit at the IRCCS Istituto Neurologico Mediterraneo Neuromed, Pozzilli (IS), Italy. He also leads the Synaptic Immunopathology Laboratory at Tor Vergata University. His major clinical interest involves the evaluation of new drugs for the treatment of MS. His research interests are related to the role of synaptic transmission and plasticity in the pathophysiology of multiple sclerosis and of its experimental model, and to the physiology of the endocannabinoid system and its involvement in inflammatory neurodegenerative diseases.
Prof. Centonze graduated in Medicine from the University of Rome La Sapienza in 1994, specialized in Neurology in 1999, and in Psychiatry in 2006 at the University of Rome Tor Vergata. He completed his PhD in Rehabilitation Medicine in 2012.
He is the principal investigator of many phase II, III, and IV national and international trials with new therapeutic agents for MS. He was awarded several research grants by the Italian Ministry of Health, the Italian Ministry of Education, Universities, and Research, the Italian Ministry of Defence, the Multiple Sclerosis Italian Foundation, and the European Commission.
Prof. Centonze is the author of around 370 peer-reviewed papers published in international journals of Neuroscience, Neurology, and Psychiatry.