Profile of galectins at the maternal-fetal interface in HIV-1 infection

• Grant number: 23/16264-9
• Support Opportunities: Scholarships in Brazil - Master
• Start date: March 01, 2025
• End date: June 30, 2026
• Field of knowledge: Biological Sciences - Immunology - Applied Immunology
• Principal Investigator: Maria Notomi Sato
• Grantee: Gabriela Domingues Mattos
• Host Institution: Faculdade de Medicina (FM). Universidade de São Paulo (USP). São Paulo , SP, Brazil
• Associated research grant: 19/25119-7 - Maternal-fetal interface: immunopathogenesis and vaccinal intervention in viral infections, AP.TEM
• Associated scholarship(s): 25/08119-4 - Placental Galectin Signatures in HIV-1-Positive Women: Spatial Distribution and Glycosylation Patterns, BE.EP.MS

Abstract

Immune tolerance at the maternal-fetal interface is essential for fetal development and in controlling the response to infectious agents, such as Human Immunodeficiency Virus type 1 (HIV-1). Several mechanisms mediated by cells and/or factors act in gestational tolerance to control the generation of responses to alloantigens and also for immunity to infections that may occur at this stage. Galectins (gal) are defined as lectins, that is, proteins capable of binding to carbohydrates and that can bind to glycans on the surfaces of viruses, bacteria and fungi. They largely act as a control protein for cell-cell interactions, adhesion, proliferation, apoptosis, immunity and inflammation. The project proposal is to analyze the expression profile of galectins in the placenta and umbilical cord cells, in HIV-1 infection. Furthermore, verify the immunoregulatory potential of galectins in the production of cytokines in newborn cells. To this end, fifteen galectins will be analyzed in the villous and decidual layer of placentas by qPCR and the protein expression of gals that play a role in the placenta (gal-1, gal-3, gal-9 and gal-13). Furthermore, the presence of these galectins will be analyzed in umbilical cord mononuclear cells and for their in vitro regulatory effect on the production of cytokines induced by TLR4 agonists. Immunomodulation by galectins in the anti-inflammatory or immunoregulatory context will be crucial to attenuate maternal HIV-1 immunoactivation and useful in identifying markers in the regulation of the maternal-fetal interface.