Chargé de Recherche-CR1 (Equivalent of Associate Professor) at Institut National de la Santé et de la Recherche Médicale (INSERM) (French National Institute of Health and Medical Research).
2010-: Chargé de Recherche-CR1 (Equivalent of Associate Professor) at Institut National de la Santé et de la Recherche Médicale (INSERM).
2010-: Expert Member of AERES (L'agence d'Evalution de la Recherche et de l'Enseignement Supérieur) (French Agency for Evaluation of Research and Higher Education)
2009-: Appointment to Panel LS6 "Immunity and Infection" evaluation referee panel of European Research Council (ERC) for 5 years (2009-2013)
2006-10: Chargé de Recherche-CR2 (Equivalent of Assistant Professor) at Institut National de la Santé et de la Recherche Médicale (INSERM).
The maintenance of immune equilibrium and optimum immune response to pathogens implicate a co-coordinated cross-talk between antigen presenting cells such as dendritic cells (DCs), and cells of adaptive immunity T and B cells. In addition to DCs, the most potent and efficient professional antigen-presenting cells (APCs), specific T-cell populations with suppressive/regulatory properties such as CD4+CD25+ regulatory T cells (Tregs) are devoted to the maintenance of antigen-specific T-cell tolerance. A dysregulation in the dialogue between immune mediators results in a break in the immune tolerance leading to immunopathological situations including autoimmunity.
My research activities are focused on understanding immune tolerance and deciphering host-pathogen interactions.
I am conducting research on how circulating IgG (by using therapeutic intravenous immunoglobulin, obtained from pooled plasma of thousands of healthy donors) and Tregs are devoted to the maintenance of tolerance upon interaction with innate (such as dendritic cells) and adaptive immune cells (such as T and B cells).
I have designed small molecule adjuvants that target CCR4 on regulatory T cells (Tregs). These molecules transiently block Treg migration without depleting them and allowing antigen presenting cells to enhance the efficacy of vaccines. These results have been acclaimed as a milestone and being exploited by several labs and industry for clinical applications.
My research program also concerns understanding the molecular interaction of cell wall antigens of two human pathogens-Aspergillus fumigatus and Mycobacterium tuberculosis with antigen presenting cells and its repercussion on adaptive immune responses. A. fumigatus is a mold that causes the most prevalent and lethal human systemic fungal infections worldwide and Mycobacterium tuberculosis is the etiologic agent of tuberculosis and a leading cause of death worldwide. I have recently shown that hydrophobin layer on the surface of airborne fungal conidia accounts for their inert nature thus preventing unwanted deleterious immune responses to thousands of fungal conidia that we breathe in our daily life. These observations have been published in NATURE and are subjected to several intense ongoing studies under ANR, FP7 programs and international collaborative efforts.
Taken together, I insist on intensifying the interaction between fundamental research and clinical research.