Since 2008 : Assistant Professor (UMR_S 1064, Nantes, France).
Recruited as an assistant professor in 2006 (CR1 INSERM - CIRID, Bordeaux).
Postdoct fellowships: 2000-2006 (CIRID and Avenir team as a team leader in Bordeaux, France).
Cursus: University of Nantes, Faculty of Sciences and Technology (Master degree in Biochemistry and Immunology), School of medecine (PhD Immunology in 1999).
Member of the « Club Francophone des Cellules Dendritiques » (CFCD) and of the French Society for Microbiology (SFM).
Some years ago, I demonstrated that the cytomegalovirus (CMV) infection of monocyte-derived dendritic cells (MDDCs) was strongly promoted by the C-type lectin DC-SIGN. Once infected, DCs may behave as a Trojan horse and thus participate to the viral spreading and most likely to the latency setup since myeloid cells are one of the two major cellular reservoir for the CMV in humans. A recent study by my group reported that CMV was internalized by macropinocytosis thus leading to the protection of the CMV particles for several hours in an endosomal compartment. These hidden particles kept their infectious potential and had the ability to go out and infect proximal target cells.
Based on the literature and on own work, we hypothesized that in vivo tissue-residing DC might behave distinctly toward a CMV primary challenge compared to MDDCs. In order to better delineate the role of myeloid DCs and their cell-surface lectinic receptors in the CMV primary infection, we sought to develope an organotypic model of human mucosa containing MDDCs and MDLCs (monocyte-derived Langerhans cells) to study their contribution to a primary challenge with CMV.
In this setting, we also developed new lentiviral vectors to improve gene transfer into MDDCs/MDLCs in collaboration with another French group headed by F-L Cosset and E Verhoeyen (INSERM, EVIR, UMR758/ENS Lyon, France). As a corollary, my group has an interest in developing new pseudotype for lentiviral vectors (LVs) with the aim to improve the human DC transduction specificity/efficiency.
Recently, my group started to develop new strategies to inactivate CMV and other pathogenic herpesvirus family members in a transplantation setting.