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  • Phone : +3368380797
  • Location : Marseille, France
Last update 2015-07-30 10:26:08.196


Course and current status

2015-        : PhD student in Lena Alexopoulou's laboratory, Centre d'Immunologie de Marseille-Luminy

2013-2015: Master of Science in Biology, Ecole Normale Supérieure de Lyon

-> Internship in Lena Alexopoulou's laboratory, Centre d'Immunologie de Marseille-Luminy

-> Internship in Julie Déchanet-Merville's laboratory, CIRID, Bordeaux

-> Internship in Thomas Henry and Benedicte Py's laboratory, International Center for Infectiology Research, Lyon 

2012-2013: Bachelor of Science in Biology, Ecole Normale Supérieure de Lyon

Scientific summary

Toll-like receptors in immunity 

    Toll-like receptors (TLRs) are transmembrane pattern recognition receptors and are expressed in various immune cells including macrophages and dendritic cells. The TLR family is composed of 10 members in humans and 12 members in mice, of which TLR1-TLR9 are found in both species. TLRs can be divided into two groups: those located at the plasma membrane are activated by microbial membrane lipids or bacterial proteins, while the TLRs in the endolysosomal compartment (TLR3, TLR7, TLR8 and TLR9) recognize microbial nucleic acids. Upon ligand binding, TLRs trigger signaling pathways, leading to the induction of inflammatory and innate antimicrobial immune responses. There are increasing evidence that intracellular TLRs can also recognise self-antigens released from damaged or stressed host tissue and that such recognition can lead to the development of autoimmune diseases, including systemic lupus erythematosus.

    Although TLR7 and TLR8 are phylogenetically and structurally related, their natural ligand viral single-stranded RNA stimulates human TLR7 and TLR8 and mouse TLR7, but not mouse TLR8, leading to the belief that TLR8 is biological inactive in mice. However, recent work of the host team demonstrated an important and previously unidentified role for TLR8 in the regulation of TLR7-mediated autoimmunity in mice. TLR8 restrain TLR7 function and TLR8-deficient mice develop lupus autoimmunity due to increased TLR7 expression and signalling (Demaria et al, J Clin Invest, 2010).


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