IL-27 expression and its role in the progression of Canine Leishmaniasis

• Grant number: 19/18252-2
• Support Opportunities: Scholarships in Brazil - Doctorate
• Start date: June 01, 2020
• End date: May 31, 2023
• Field of knowledge: Agronomical Sciences - Veterinary Medicine
• Principal Investigator: Valéria Marçal Felix de Lima
• Grantee: Marilene Oliveira dos Santos Maciel
• Host Institution: Faculdade de Medicina Veterinária (FMVA). Universidade Estadual Paulista (UNESP). Campus de Araçatuba. Araçatuba , SP, Brazil

Abstract

Visceral Leishmaniasis (VL) is a chronic disease and often fatal if left untreated. It is expanding with high mortality rate, and the region of Araçatuba concentrates a high number of cases in the state. Canine Visceral Leishmaniasis (CanL) is a serious public health problem because infected animals are powerful transmitters of the parasite to humans by the phlebotomine vector, and canine disease is more prevalent than human disease and usually canine cases precede human cases. The dog is, therefore, an important target in control measures. The progression of canine infection is accompanied by failure in cellular immunity with reduction of circulating lymphocytes and cytokines that suppress macrophage function. The role of the T cell in inducing the cellular response is crucial for the elimination of the parasite within macrophages. Although immune suppression is already characterized, the determining factors are poorly known. In the last decade, studies have shown that regulation of effector T-cell function seems to depend on IL-27. There is evidence of the role of IL-27 in regulating the expression of cytokines involved with disease progression, besides, the inefficient cellular immune response in Canine Leishmaniasis may be a result of IL-27 action which in other models increases PD1 expression. , which leads to exhaustion of T cells. Thus we will evaluate if the progression of the canine disease is associated with IL-27 and how IL-27 acts in the regulation of cytokines and costimulators in Canine Leishmaniasis. Our results will improve our understanding of the pathogenesis of VL in the host, and as such, reveal new pathways that may constitute therapeutic targets. (AU)