Toll Like Receptors function as pathogen recognition receptors, sensing a wide range of invading pathogens through recognition of pathogen-associated molecular patterns (PAMPs). Engagement of TLRs by microbial products triggers the activation of two downstream signalling pathways: the MyD88-dependent and -independent (or IRF3-dependent) pathways, leading to inflammatory responses. Recent evidence suggests that Protein Kinases C (PKC) are key regulators of these signaling pathways. For example, generation of PKCe deficient mice revealed a major defect in the ability of  PKCe ^-/- macrophages to generate inflammatory mediators in response to LPS. In vivo, these mice showed susceptibility to Gram-positive and Gram-negative infection. PKCd  deficient macrophages present an impaired activation of NF-kB and MAPK downstream of TLR2 and TLR4. Recently, Christelle Langlet and her research team showed that conventional PKCα plays a critical role in IRF3 activation and IFN-β synthesis downstream of TLR3. Directed by this previous work, their investigated the implication of conventional PKCα isoform in the MyD88-dependent signalling pathway. In vitro results obtained on human dendritic cells, murine dendritic cells and a recombinant HEK293 cells system will be presented.