Rab14 regulates antigen presentation by major histocompatibility complex type I (MHC-I) in dendritic cells infected with Chlamydia trachomatis

CAPMANY A; CEBRIAN I; DAMIANI MT

Puerto Varas

Congreso; XII PABMB CONGRESS-XXXVI ANUAL MEETING SOCIEDAD DE BIOQUÍMICA Y BIOLOGÍA MOLECULAR DE CHILE-XLIX ANUAL MEETING DE LA SOCIEDAD ARGENTINA EN BIOQUÍMICA Y BIOLOGÍA MOLECULAR-LV1 ANUAL MEETING SOCIEDAD DE BIOLOGÍA DE CHILE-4 LATIN AMERICAN PROTEIN SOCIETY; 2013

Pan-American Association for Biochemistry and Molecular Biology and SAIB

Chlamydia is an obligate intracellular bacterium that replicates inside a vesicle called inclusion. This pathogen manipulates Rab GTPases, master controllers of vesicular transport, to ensure its survival and replication. Dendritic cells are the most powerful antigen presenting cells of the immune system. We have shown that Chlamydia trachomatis intercepts Rab14-vesicles to acquire host lipids necessary for its growth and multiplication. Recently, it has been determined that an efficient cross-presentation requires that the exogenous antigen containing-phagosome interacts with Rab14-endosomes. Our hypothesis is that C. trachomatis recruits Rab14 not only as a strategy for nourishment, but also to interfere with the process of antigen presentation. By confocal microscopy, we observed that the transferrin receptor (RTf) is recruited to the inclusion immediately after bacterium invasion and remains throughout its development. Furthermore, we observed that Rab14 is associated with the plasma membrane at the entry site of the bacterium. Later, Rab14 is recruited to the chlamydial inclusions and remains throughout the entire cycle. The knock-down of Rab14 impairs the bacterial invasion. In addition, Rab14 silencing causes a redistribution of MHC-I molecules and interferes with their transport towards the plasma membrane, assessed by flow cytometry. These data suggest that Rab14 plays a role not only for bacterial growth but also for its hiding from immune system