Leticia Sampedro de la Fuente
Leticia Sampedro de la Fuente
ANIMAL UNIT TECHNICIAN
Inflammation and Macrophage Plasticity Lab & Animal Facility
Address: Bizkaia Science and Technology Park, building 801A, Derio (Bizkaia)

The macrophage and tick vaccine laboratory studies the interaction between athropod vectors, infectious microorganisms and their mammalian hosts. The laboratory is primarily focused on ticks of the genus Ixodes, which transmit several medically important pathogens, such as the causative agent of Lyme borreliosis, Borrelia burgdorferi. The lab participates in a large multicenter project funded by the EU (ANTIDotE) that seeks to identify tick salivary antigens that could be used as potential vaccine candidates against tick bites and therefore, prevent the transmission of pathogens. They are also interested in the pharmacological activities exerted by tick saliva proteins, especially those that can modulate the immune response and that can have therapeutic applications in immune disorders. Finally, the group is interested in understanding the regulation of the immune response pathways present in ticks that participate in the control of pathogens within the vector.
On the other hand, the laboratory seeks to understand the response of macrophages to infectious agents, from Lyme borreliosis to inflammatory bowel disease to tuberculosis. They are interested in understanding the metabolic control of macrophage responses through the specific mitochondrial complex I repressor, MCJ in different models of disease in which these cells participate, such as Lyme carditis and inflammatory bowel disease. Furthermore, the role of INFγ and other signals on the plasticity of the response of macrophages to infectious agents is another focus of the laboratory. Finally, the group is interested in defining the phagocytic ‘ome’ that mediates the uptake, elimination and initiation of proinflammatory responses by macrophages. In this context, the group described the Complement Receptor (CR) 3 as a phagocytic receptor involved in the elimination of B. burgdorferi by macrophages. CR3 cooperates with the GPI-anchored protein, CD14, in the internalization of the spirochete, a novel mechanism that is independent of MyD88 signals.