Jamel El Benna

Name : Jamel EL BENNA. **Title and position:**PhD, Research Director at CNRS. **Laboratory:** INSERM-U1149, CNRS-ERL8252,Center of Research on Inflammation (CRI), Team « Phagocytes, NADPH Oxidases and Immunogenetics in Systemic Inflammation » Faculté de Médecine Xavier Bichat, 16 rue Henri Huchard 75018 Paris, France, Tél: 01 57 27 77 23, Email : jamel.elbenna@inserm.fr **Education/Training:** University Paris 11 Orsay - Master’s degree - (1988) - Biochemistry and Immunology University Paris 11 Orsay – PhD - (1992) - Biochemistry and Immunology Scripps Research Institute, La Jolla, CA, USA - Postdoctoral - (1992-1995) - Biochemistry University Paris 7 - HDR - (2003) - Biochemistry and Immunology **Personal Statement:** Reactive oxygen species (ROS) play a critical role both in host defense and in induction of pathological inflammatory processes. So far only limited information is available as to how ROS production becomes out of control in inflammatory diseases. A better knowledge of the different steps that participate in the initiation and termination of the production of ROS is required to further understand the mechanisms that lead to deregulation of their production in inflammatory diseases. For years, I have been interested in the pathways involved in the activation and regulation of the phagocyte NADPH oxidase/NOX2. P47phox is a critical cytosolic component in the organization of the active NOX2. My work has identified the p47phox phosphorylated sites and demonstrated their functional importance. We have also showed that the proinflammatory cytokines TNFalpha and GM-CSF which induce NOX2 hyperactivation or priming, are able to induce the phosphorylation of p47phox on a specific site. We produced an antibody against phospho-p47phox, interestingly, the antibody we developed allowed us to detect hyper-phosphorylation of p47phox in neutrophils from synovial fluids obtained from patients with rheumatoid arthritis (RA). We also developed a peptide composed of a peptide vector and a p47phox amino acid sequence. This peptide inhibits the hyperactivation of neutrophils induced *in vitro* by TNF and GM-CSF and the hyperactivation of neutrophil from synovial fluids of RA patients. We have also shown that the proline isomerase Pin1 is involved in TNF-induced NOX2 hyperactivation by binding to phospho-p47phox. **Position and Employment:** 1995-2006: Research Scientist (CR1) at CNRS. 2006-present : Research Director (DR2 and DR1) at CNRS. **Scientific functions:** Supervisor of a research group in INSERM U479 unit (1998-2004) Supervisor of a research group in INSERM U683/U773 unit (2005-2008) Supervision of 8 thesis ; examiner of 10 thesis Scientific Expertise for : ANR, INSERM, CNRS, Swiss Science Fondation. Organisation of 3 meetings. Member of the editorial Board: Biochem. Pharmacol, Open J.Inflammation,Am.J.Blood Research. Referee for scientific reviews (JBC,Blood,J.Immunol,J.Leuk.Biol,EMBOJ, Biochem.Pharmacol) Member of the scientific committee of “bio-therapy.net“ site Member of the faculté X.Bichat executive board (2000-2004). **Teaching :** 3 Masters (University Paris 7-Saint Louis, University Paris 7-Bichat, University Paris 11-Orsay). **Grants and patents :** grant from ANR (2008-2010), ARC (2 contrats), ARP (4 contrats), American Arthritis Foundation Award (USA), patent (US60/774,653 ; 60/774,653). **Membership :** American Society for Biochemistry and Molecular Biology (ASBMB), American Association for the Advancement of Science (AAAS), The Society for Free Radical Research International (SFRRI). **Publications and communications:** (For PubMed search please use “Benna J”): 166 publications, 14 book chapters, 150 abstracts, 44 invited speaker.