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The participation of innate immune receptors in the autophagy induction in response to Trypanosoma cruzi infection.

Grant number: 12/02786-9
Support Opportunities:Scholarships in Brazil - Doctorate
Effective date (Start): June 01, 2012
Effective date (End): February 29, 2016
Field of knowledge:Biological Sciences - Immunology - Cellular Immunology
Principal Investigator:Dario Simões Zamboni
Grantee:Catarina Veltrini Horta
Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
Associated scholarship(s):15/04596-0 - Generation of gene-deficient mice by using CRISPR/Cas genome editing, BE.EP.DR


Chaga's disease, caused by Trypanosoma cruzi protozoan, is one of the most serious parasitic disease in Latin America, affecting approximately 10 million people. The control of infection by mammalian hosts is dependent on effective immune recognition of the parasites by innate immune cells such as macrophages and dendritic cells. These cells express pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs) and Nod-like receptors (NLRs) that account for pathogen recognition and generation of effective immune responses, such as autophagy process. This process is considered an emerging effector mechanism in the pathogen elimination by innate immune cells. On the order hand, the role of autophagy during T. cruzi infection is unclear. In this context, we aim to investigate the role of autophagy in response to T. cruzi infection. Furthermore, we aim to evaluate the role of innate immune receptors in the autophagy induction in response to T. cruzi infection.

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