M. tuberculosis is recognized by several Pattern Recognition Receptors (PRRs), including TLRs and C-type lectins, allowing its detection by the innate immune system. However, the pathogen is able to undermine innate immune responses, including inflammatory response and autophagy, thus favoring its survival inside the infected host.
Our main working axes are:
- Molecular bases of M. tuberculosis recognition by PRRs (TLR2, DC-SIGN, Mincle, Dectin-1, Dectin-2), identification and structural characterization of M. tuberculosis ligands (PAMPs).
- Molecular mechanisms used by Mtb to inhibit innate immune responses.
- Rational design of synthetic analogs of mycobacterial immunomodulatory molecules with the objective of developing adjuvants or anti-inflammatory agents: mode of action and therapeutic potency.
- Autophagy modulation by mycobacterial lipids.
- M. tuberculosis lipid trafficking within extracellular vesicles and remodeling of M. tuberculosis lipidome during infection.