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Characterization of the role of Interleukin-27 (IL-27) during Leishmania infantum infection

Grant number: 13/08313-8
Support type:Scholarships in Brazil - Master
Effective date (Start): October 01, 2013
Effective date (End): January 31, 2015
Field of knowledge:Biological Sciences - Immunology - Cellular Immunology
Principal researcher:João Santana da Silva
Grantee:Gustavo Fernando da Silva Quirino
Home Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
Associated research grant:12/14524-9 - Modulation of T lymphocytes differentiation in infections by Protozoa, Fungi and Bacteria, AP.TEM

Abstract

The genus Leishmania is composed by several protozoans which cause a complex of diseases called leishmaniasis. Visceral leishmaniasis (VL) is a systemic, chronic and potentially fatal disease caused by L. infantum, endemic in Brazil. This parasite is transmitted through the bite of phlebotomies insects, and promastigotes inoculated rapidly infect macrophages, disseminating to the spleen, liver, lymph nodes and bone marrow thereafter. The immune response is crucial to control the parasite, being macrophages and dendritic cells key players during Leishmania infection, once that they are infected and stimulated adaptive responses. This response is mainly cellular, and Th1 lymphocytes are classically regarded as protective, through IFN-g production, as well as Th17 through IL-17 secretion. On the other hand, IL-10, produced by several cell types, can act suppressing the response against this pathogen, allowing for disease establishment. Recently, it has been observed that, during L. donovani infection, CD4+ T cells committed to the Th1 lineage can acquire, after IL-27 and IL-10 stimulus, a Tr1 phenotype, characterized by production of IL-10, which favors the host susceptibility. However, the role and participation of these cells and cytokines during L infantum infection has not been showed. The aim of this work is to evaluate the participation of IL-27 in adaptive immune response during VL. Further, this work can collaborate for the development of therapeutic interventions to control this disease.

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