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The role of indoleamine 2, 3-dioxygenase 1 (IDO-1) in immunosuppressive mechanisms of myeloid-derived suppressor cells (MDSCs) in Pulmonary Paracoccidioidomycosis

Grant number: 19/24440-6
Support type:Scholarships in Brazil - Post-Doctorate
Effective date (Start): March 01, 2020
Effective date (End): February 28, 2022
Field of knowledge:Biological Sciences - Immunology - Applied Immunology
Principal researcher:Flávio Vieira Loures
Grantee:Valéria de Lima Kaminski
Home Institution: Instituto de Ciência e Tecnologia (ICT). Universidade Federal de São Paulo (UNIFESP). Campus São José dos Campos. São José dos Campos , SP, Brazil
Associated research grant:18/14762-3 - Immunosuppression in paracoccidioidomycosis: the regulatory role of myeloid-derived suppressor cells (MDSCs) on host immunity, tissue pathology and genetic adaptation of fungal cells, AP.JP2

Abstract

Previous studies in Paracoccidioidomycosis (PCM), the most prevalent systemic mycosis in Latin America, revealed that immunity of hosts is tightly regulated by several suppressive mechanisms mediated by tolerogenic plasmacytoid dendritic cells, the enzyme 2,3 Indoleamine Dioxygenase (IDO1) and regulatory T cells (Treg). IDO1 was also seen to orchestrate local and systemic immunosuppressive effects through the recruitment and activation of Myeloid-Derived Suppressor Cells (MDSCs), a heterogeneous population of myeloid cells with a potent ability to suppress T cell responses. These cells regulate immune responses and tissue repair in healthy individuals and rapidly expands during infection. The involvement of MDSCs during PCM was never investigated, leading us to propose this study that aims to characterize the participation of MDSCs in the immunity against P. brasileinsis infection. The presence, phenotype and activity of MDSCs will be evaluated at several post infection periods. Based on previous studies that established a positive correlation between IDO activity and MDSC infiltration we also intend to do a comparative study on MDSCs function in pulmonary PCM using IDO-deficient and sufficient-mice. A better understanding of immunoregulation in pulmonary PCM mediated by MDSCs will possibly advance the current knowledge of the host-pathogen responses that control the severity of PCM and will open new perspectives for more effective therapies. (AU)

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