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Role of MYD88 and caspase-1 in the induction of autophagy and its relevance to the control of T. cruzi infection

Grant number: 12/10077-8
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Effective date (Start): September 01, 2012
Effective date (End): July 31, 2013
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
Associated research grant:08/50958-8 - Interaction between innate immune receptors in the activation of macrophages and dendritic cells, AP.JP


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 for the lack of these components. In infectious processes, autophagy helps in the control of microorganisms, which are involved by autophagosomes that fuse to lysosomes, responsible for the degradation of the captured microorganism. The molecular patterns recognition receptors (PRRs) of innate immunity have been related to the regulation of the autophagy process and the control of microorganisms. In this sense, the toll-like receptors (TLR) activate the process of autophagy, while the cytosolic receptors, such as the inflammasomes, negatively regulate this process. Since both the TLR receptors and the inflammasomes 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 TLR and inflammasomes in the regulation of autophagy and its impact on macrophage's ability to kill this parasite.(AU)

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