Biosketch

My research focuses on the interactions between the gut microbiome and the innate immune system in various organ-specific autoimmune diseases and beyond. During my PhD at the National Institute of Health and Medical Research (INSERM), I worked in Unit 346 under the supervision of Prof. Daniel Schmitt, I examined the impact of Toxoplasma gondii on human dendritic cells (DCs). We discovered that this parasite has evolved multiple strategies to manipulate human DC function and evade the immune response. 

I undertook my postdoctoral training at INSERM Unit 561 from 2006 to 2011 under the direction of Agnes Lehuen. My postdoctoral project involved studying the role of DCs during viral infection in a mouse model of autoimmune diabetes. We demonstrated that a subset of DCs (i.e. plasmacytoid DCs (pDCs)) played a pivotal role in preventing autoimmune diabetes induced by viral infection. We demonstrated that virally activated pDCs induced the expansion of regulatory T cells, which reduced the diabetogenic response in non-obese diabetic (NOD) mice (J. Exp. Med. 2011; Immunity 2009). 

In 2011, I was appointed as a permanent researcher at INSERM. I initiated a project investigating the role of innate immune cells in the development of autoimmune diabetes in a non-infectious context in mice. We uncovered a previously unknown mechanism by which autoimmune diabetes is initiated and demonstrated the hitherto unknown role of neutrophils in this disease (Nat. Med. 2013). This study is a significant step towards the future development of novel clinical approaches based on the manipulation of innate immune cells to prevent autoimmune diabetes. 

In 2013, I established my research group at the Institut Necker Enfants Malades (INEM) and began an original project investigating the role of antimicrobial peptides (AMPs) in autoimmune diabetes. We demonstrated that, under the control of the gut microbiota, pancreatic endocrine cells express antimicrobial peptides that maintain immune tolerance in the pancreas (Immunity, 2015; Cell Metabolism, 2018). We also demonstrated the role of a specific intestinal AMP in establishing a healthy gut microbiota in newborn mice and investigated whether defects in the expression of this peptide are involved in the development of autoimmune diabetes. We demonstrated that an AMP-expressing probiotic effectively corrects the gut microbiota and prevents the development of autoimmune diabetes (Gastroenterology, 2022). In a recent study, we extended these findings to another autoimmune disease (i.e. multiple sclerosis), and we showed the protective role of brain-born AMPs in controlling neuroinflammation (J. Clin. Invest., 2024). 

Our current projects aim to explore the interaction between the gut microbiota, the innate immune system, and non-immune cells in the context of autoimmunity and beyond, as well as how AMPs serve as messengers in this interaction and could be used as therapeutic tools.