Isabelle Vergne
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Project: Autophagy & Infection
Autophagy is an eukaryotic lysosomal degradative process that plays major roles both cellular homeostasis and the immune system during infection. We are interested in investigating the molecular and cellular interaction between this process and pathogenic bacteria with a focus on Mycobacterium tuberculosis.
The three main goals of our research are:
– To identify and characterize bacterial and host factors involved in autophagy regulation
– To decipher the functions of autophagy and autophagy-related genes during infection
– To develop novel vaccines against M.tuberculosis based on autophagy
Overall, our work should bring new insights into the intricate interplay between host autophagy and pathogenic bacteria. This better understanding could help in designing innovative prophylactic and curative therapeutics based on autophagy manipulation for the fight against tuberculosis and other pathogens.
Autophagy is an eukaryotic lysosomal degradative process that plays major roles both cellular homeostasis and the immune system during infection. We are interested in investigating the molecular and cellular interaction between this process and pathogenic bacteria with a focus on Mycobacterium tuberculosis.
The three main goals of our research are:
– To identify and characterize bacterial and host factors involved in autophagy regulation
– To decipher the functions of autophagy and autophagy-related genes during infection
– To develop novel vaccines against M.tuberculosis based on autophagy
Overall, our work should bring new insights into the intricate interplay between host autophagy and pathogenic bacteria. This better understanding could help in designing innovative prophylactic and curative therapeutics based on autophagy manipulation for the fight against tuberculosis and other pathogens.
Animal and Cellular models:
Cell lines (RAW 264.7, THP-1), primary macrophages
Cell lines (RAW 264.7, THP-1), primary macrophages
Techniques and Methods:
Autophagy methods
Autophagy methods