PD1 in regulation of parasite load and NO production from spleen leucocytes dogs with Visceral Leishmaniasis

• Grant number: 16/11494-2
• Support type: Scholarships in Brazil - Scientific Initiation
• Effective date (Start): January 01, 2017
• Effective date (End): December 31, 2017
• Field of knowledge: Biological Sciences - Immunology - Cellular Immunology
• Principal researcher: Valéria Marçal Felix de Lima
• Grantee: Lucas Takeshi Siqueira Ito
• Home Institution: Faculdade de Medicina Veterinária (FMVA). Universidade Estadual Paulista (UNESP). Campus de Araçatuba. Araçatuba , SP, Brazil

Abstract

The visceral canine leishmaniasis (VCL) is one of the most important emerging diseases, with high prevalence in countries of latin america, and It is caused mainly by Leishmania (L.) chagasi. The VCL has a great effect about public health, in virtue of domestic dogs being the most important disease reservoirs, both in urban areas as peri-urban. So the dog is an important target for the adoption of control measures. The progression of canine infection is accompanied by failure in cellular immunity. The macrophages plays an important role in immune response against Leishmania spp., because they are parasitized cells and can trigger the adaptive response. The T cell is responsible for activating the macrophage engaged in its receptor TCR to MHC associed to the antigen of parasit phagocyted by the macrophage. Along with further signals connection of costimulatory molecules on the surface of both cells, the effector function of the interaction will take place. The macrophages may allow the multiplication of the parasite or exercise the leishmanicida activity by the production of NO. PD1, an inhibitory costimulatory is involved with cells T exaustion. It regulatory role in parasite load and NO production in blood cells have been observed, but the primary affected organ spleen was not studied. Thus intends to verify in naturally infected dogs if the splenic parasitic load and NO production are changed by the PD- 1 receptor blockade of CD14 + cells. (AU)