2004-2008 PhD student in immunology, Angers, France
2003-2004 Master’s degree in Cell Biology and Immunology, Poitiers, France
2014-present Post-doctoral research associate Milan, Italy
- HMGBiotech, R&D division, San Raffaele Scientific Institute, Pr. ME Bianchi
- Research projects
“A non-oxidizable form of HMGB1 as a candidate for muscle repair therapies”
“Identification of new drugs for modulation of HMGB1 secretion”
2008-2013 Post-doctoral fellow in immunology Milan, Italy
- DIBIT San Raffaele Scientific Institute, Chromatin Dynamics Unit, Pr. ME Bianchi
- Research projects
“Study of HMGB1 involvement in inflammation and tissue repair”
- Teaching : Molecular cell biology to international MD students, San Raffaele, Milan, Italy
2004-2008 PhD Student Angers, France
- INSERM Unit 564, “Cytokines: structure, signalling and tumoral proliferation”, Dr H.Gascan
- Research projects
“Development of fused soluble receptors neutralizing biological functions of cytokines”
“Study of cytokine involvement in skin inflammatory diseases and tumoral cell proliferation”
- Teaching : Molecular biology to « Innovations in biotechnology » Master students, ISTIA, Angers, France
2003-2004 Master’s degree student, Angers, France
- INSERM Unit 564, “Cytokines: structure, signalling and tumoral cell proliferation”, Dr. H. Gascan
- Research project
“Generation of a fused soluble receptor antagonizing properties of Interleukin-31 ”
US provisional patent application N. 61/676,071 (priority date: July 26th, 2012) entitled “HMGB1 variants and uses thereof” (inventors: Marco Emilio Bianchi, Emilie Vénéreau, Maura Casalgrandi; applicant: Ospedale San Raffaele srl).
Present Grant from Ministero della Salute (Giovani ricercatori)
2011-2013 Fellowship from FIRC (Italian foundation for cancer research)
2007-2008 Fellowship from Association pour la Recherche sur le Cancer
2004-2007 Fellowship from Ministère de la recherche
Our body detects pathogens via a set of receptors that recognize pathogen-associated molecular patterns (PAMPs) and trigger the response of the immune system. The damaged tissues also release intracellular molecules, Damage-Associated Molecular Patterns (DAMPs), which activate the immune system. DAMPs represent sophisticated molecules essential for protection of the host and tissue healing, but in turn they can cause tissue damage and disease. Since 15 years, a growing body of studies have been focused on the identification of DAMPs and their roles in health and disease.
We are particularly interested in HMGB1 biology because this protein fits exemplarily all of the criteria for DAMPs. This nuclear protein is released by dead or stressed cells, but not by apoptotic cells. HMGB1 signals “danger” to surrounding cells and triggers inflammation and innate immunity to stop the damage. Finally, it contributes to tissue repair and healing. Extensive evidence reveals an essential role for HMGB1 in both infection- and injury-elicited inflammatory diseases.
– Venereau E, Schiraldi M, Uguccioni M, Bianchi ME. HMGB1 and leukocyte migration during trauma and sterile inflammation. Mol Immunol 2013 Aug;55(1):76-82.
– Venereau E, Casalgrandi M, Schiraldi M, Antoine DJ, Cattaneo A, De Marchis F, Liu J, Antonelli A, Preti A, Raeli L, Shams SS, Yang H, Varani L, Andersson U, Tracey KJ, Bachi A, Uguccioni M, Bianchi ME. Mutually exclusive redox forms of HMGB1 promote cell recruitment or proinflammatory cytokine release. J Exp Med. 2012 Aug 27;209(9):1519-28.
– Schiraldi M, Raucci A, Martínez Muñoz L, Livoti E, Celona B, Venereau E, Apuzzo T, De Marchis F, Pedotti M, Thelen M, Varani L, Mellado M, Proudfoot A, Bachi A, Bianchi ME and Uguccioni M. HMGB1 promotes recruitment of inflammatory cells to damaged tissues by forming a complex with CXCL12 and signaling via CXCR4. J Exp Med. 2012 Mar 12;209(3):551-63.
– Yang H, Lundbäck P, Ottosson L, Erlandsson-Harris H, Venereau E, Bianchi ME, Al-Abed Y, Andersson U, Tracey KJ, Antoine DJ. Redox modification of cysteine residues regulates the cytokine activity of HMGB1. Mol Med. 2011 Mar 30;18(1):250-9.
– Mittal D, Saccheri F, Venereau E, Pusterla T, Bianchi ME, Rescigno M. TLR4 mediated skin carcinogenesis is dependent on immune and radioresistant cells. EMBO J. 2010 Jul 7;29(13):2242-52.