Mechanisms that regulate the processing of IL-1a, IL-1b and their role during experimental Trypanosoma cruzi infection

• Grant number: 14/25585-4
• Support Opportunities: Scholarships abroad - Research Internship - Post-doctor
• Start date: February 28, 2015
• End date: February 27, 2016
• Field of knowledge: Biological Sciences - Immunology - Cellular Immunology
• Principal Investigator: João Santana da Silva
• Grantee: Grace Kelly da Silva
• Supervisor: Douglas Taylor Golenbock
• Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
• Institution abroad: University of Massachusetts Medical School (UMMS), United States
• Associated to the scholarship: 13/00579-9 - Role of inflammasomes and IL-1 in experimental infection by Trypanosoma cruzi, BP.PD

Abstract

The parasite Trypanosoma cruzi is agent causative of Chagas disease. This pathogen causes robust innate immune responses in immunocompetent hosts, resulting in the recruitment of mononuclear cells to the heart. The pattern recognition receptors (PRRs), including TLR-2, -4, -7, and -9, as well as the cytosolic receptor Nod1 recognize pattern molecular pathogen associated to T. cruzi and trigger stronger immune response. Recently, we showed that inflammasomes and IL-1R are necessary for efficient control of this parasite. As both, IL-1a and IL-1b signal via the IL-1R, our goal is to elucidate the immune responses in mice lacking either of these cytokines, as to understand the mechanisms necessary to processing and release of IL-1a and IL-1b. (AU)