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Influence of PRRs in the modulation of autophagy in Trypanosoma cruzi infection and its consequences in the activation of macrophages and dendritic cells

Grant number: 13/13924-6
Support Opportunities:Scholarships in Brazil - Master
Effective date (Start): October 01, 2013
Effective date (End): July 31, 2015
Field of knowledge:Biological Sciences - Immunology - Cellular Immunology
Principal Investigator:Karina Ramalho Bortoluci
Grantee:Kely Catarine Matteucci
Host Institution: Centro de Terapia Celular e Molecular. Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil


Autophagy is a homeostatic process that occurs in the cell, where misfolded proteins and damaged organelles are degraded. This process can also occur upon lack of nutrients and energy (ATP), leading to the degradation of macromolecules to compensate the lack of these components. In infectious processes, the autophagy helps in the control of microorganisms, which are involved by autophagosomes that fuse to lysosomes, responsible for degradation of the captured microorganism.The molecular patterns recognition receptors (PRRs) of innate immunity have been related to the regulation of autophagy process and the control of microorganisms. In this sense, the toll like receptors (TLR) activate the process of autophagy, while the cytosolics receptors, such as the inflammasomes, negatively regulate this process. Since both the TLR receptors and the inflamassomas are involved in controlling the intracellular protozoan Trypanosoma cruzi, the purpose of this project is to use this infection model to investigate the influence of PRRs in the regulation of autophagy, its impact on macrophage's ability to kill this parasite and the activation of the dendritic cells and macrophages. (AU)

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