Papel de autofagia durante la transfagocitosis bacteriana en linfocitos B convencionales

Abstract

It is well established that B cells are antigen presenting cells (APC). Indeed, it is known that, in vivo, B cells are able to uptake soluble and surface-tethered antigens presented on different types of cells. However, the way B cells capture entire bacteria remains unclear. The host group recently observed that B cells are able to capture bacteria by transphagocytosis from infected dendritic cells (DC) during the B cell/infected DC contacts. Furthermore, this transphagocytic B cells (trB cells) cross-present antigens (in the Major Histocompatibility Complex I, MHC-I) from captured L. monocytogenes, potently priming naive CD8+ T cells. This process was previously described for T CD4+ T cells. The present Final Degree Project aims to elucidate whether autophagy plays an important role in trB cells-mediated antigen cross-presentation, and whether autophagy is triggered by the route by which captured bacteria are degraded. The explicit objective is comparing the induction of autophagy in trB cells. This B cells captured different strains of L. monocytogenes, able or not to escape the phagosome reaching the cytosol, and Escherichia coli, not able to escape the phagosome. The aim is to determine whether bacterial escape into the cytosol would enhance autophagy and antigen cross-presentation. The present study showed that L. monocytogenes 10403S (WT) escaping the phagosome induce autophagy in trB cells, and listeriolysin O was the main responsible for this activation. Bacteria unable to escape into the cytosol, did not induce autophagy neither antigen crosspresentation.