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Role of NLRP10 in the induction of Th1 and Th17 cells during Leishmania infantum infection

Grant number: 14/10347-0
Support Opportunities:Scholarships abroad - Research Internship - Doctorate
Effective date (Start): September 05, 2014
Effective date (End): September 04, 2015
Field of knowledge:Biological Sciences - Immunology - Cellular Immunology
Principal Investigator:João Santana da Silva
Grantee:Manuela Sales Lima Nascimento
Supervisor: Stephanie C. Eisenbarth
Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
Research place: Yale School of Medicine (YSM), United States  
Associated to the scholarship:13/01967-2 - Characterization of the mechanisms involved in the generation and modulation of protective immune response during Leishmania infantum infection, BP.DR


The visceral leishmaniasis (VL) is a systemic, chronic and potentially fatal disease caused by Leishmania infantum, endemic in Brazil. The Th1 and Th17 immune response profiles are classically associated with protection against the disease. To cope with such intracellular residing pathogens, the host has evolved sophisticated detection systems. The activation of members of the nucleotide-binding domain leucine-rich repeat containing family (NLR) is essential for the induction of innate and adaptive immune response through the antigen-presenting cells (APC) activation and soluble mediators release (i.e. cytokines, chemokines and lipid mediators). According, our results have demonstrated the importance of NOD2/RIP2 signaling pathway to induce Th1 and inhibit Th17 cells during VL, through a dendritic cell- (DC) mediated mechanism. The NLRP10 is a NLR that plays a particular role in DCs biology, as migration and cytokine production during infections, resulting in the modulation on helper T-cell-driven immune responses. Previous studies have demonstrated that NLRP10 can interact with components of NOD/RIP2 signaling suggesting that NLRP10 and NOD/RIP2 pathways may operate in synergism. Based on that, our aim is to evaluate the role of NLRP10 on the innate/adaptive immunity interface during L. infantum infection. (AU)

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