In 2015, I obtained my Bachelor degree in Molecular/Cellular Biology and Physiology at the University of Bordeaux, France. Then, I received my Master degree in Immunology and Microbiology (MIMU Master) at the University of Bordeaux, France, in 2017.
During my Master degree, I did two interships in the team of Julie Déchanet-Merville at the ImmunoConcEpT lab (Bordeaux, France). I work on gd T Lymphocyte during my first intership (2 months) and I try to experimentally challenge the Discontinuity Theory (Pradeu and Vivier, Science Immunology, 2016) during my second internship (6 months).
In 2017, I started my thesis in the Neyrolles Team at IPBS, Toulouse, France, under the supervision of Olivier Neyrolles and Yoann Rombouts. The aim of my project, founded by ANR, is to decipher the role of ST8SIA4 and Polysialic acid in macrophages during Mycobacterium tuberculosis infection.
Thanks to their strong ability to phagocyte and kill microorganisms, macrophages are key cells of the immune system, essential for protection against infection. Like all eukaryotic cells, macrophages are covered with a dense and complex array of protein- and lipid-bound glycans; yet, the contribution of these many glycans to antimicrobial defenses is largely unknown. A previous work has suggested a role of polysialic acid, a large sugar polymer synthesized by ST8SIA4, in regulating the antibacterial response of macrophages against Mycobacterium tuberculosis (Kumar et al, Cell 2010). In addition, several recent studies have demonstrated in vitro and in vivo that soluble polysialic acid polymers display anti-inflammatory properties by decreasing the production of pro-inflammatory cytokines and reactive oxygen/nitrogen species in LPS-stimulated human and mouse macrophages (Shahraz et al, Scientific Reports 2015)(Spence et al, Science Transl Med 2015). Whether or not the PolySia at the cell surface of macrophages can modulate inflammation in a same way remains to be established. In this context, my thesis aims at better understanding of the role of ST8SIA4 and polysialic acid on macrophage effector functions in response to bacterial infection.