Teresa Faria Pais

Teresa F. Pais holds a PhD in Biomedical Sciences from the University of Porto. Since 2019, she has been an Assistant Researcher at the Gulbenkian Institute for Molecular Medicine (GIMM), supported by the CEEC program of Portugal’s Science and Technology Foundation (FCT). Recently, she joined the Vector Borne Diseases Research Group at GHTM and the Medical Parasitology Unit at IHMT-NOVA.

Her early research focused on mycobacterial infections, after which she developed expertise in neuroimmunology through a Woods Hole course and training at international institutions including Dana-Farber Cancer Institute (USA) and the Theodor Kocher Institute (Switzerland). In 2008, she became a Staff Scientist at Instituto de Medicina Molecular (IMM) and subsequently a Visiting Scientist at Harvard Medical School (MGH) and the Gladstone Institutes, supported by an EMBO short-term fellowship.

Teresa F. Pais has taught Immunology as an Invited Professor at Lusófona and Católica Universities, Escola Universitária Egas Moniz, and the University of Lisbon. She has authored 29 publications and one book chapter and has served as Principal Opponent in 12 MSc and four PhD thesis defenses.

In 2024, she received funding from InnOValley and FCT to study human cerebral malaria and evaluate adjunctive therapies using cellular models.

Teresa F. Pais is primarily interested in innate immune responses within the central nervous system (CNS) under both physiological and pathological conditions. She has led FCT-funded projects investigating the role of brain macrophages (microglia) in inflammation associated with cerebral malaria and Parkinson’s disease.

Over the past decade, her research has focused on elucidating the mechanisms of brain endothelial cell activation leading to blood-brain barrier (BBB) dysfunction during cerebral malaria. Her work revealed that brain endothelial cells actively contribute to brain inflammation prior to becoming dysfunctional, by sensing Plasmodium parasites in the bloodstream through the innate immune receptor STING (Stimulator of Interferon Genes). Specifically, she demonstrated that extracellular vesicles and particles released by Plasmodium-infected red blood cells (iRBCs) deliver STING agonists to the endothelium, triggering inflammatory responses. Additionally, she is investigating whether non-canonical ligands generated during Plasmodium infection interact directly with STING and other pattern recognition receptors (PRRs). She is now using this knowledge to develop new adjunctive therapies for cerebral malaria.

1. Duarte N, Shafi AM, Penha-Gonçalves C, Pais TF. Endothelial type I interferon response and brain diseases: identifying STING as a therapeutic target. Front Cell Dev Biol. 2023 Sep 14;11:1249235. doi: 10.3389/fcell.2023.1249235. PMID: 37791071; PMCID: PMC10542901.
2. Pais TF, Penha-Gonçalves C. In vitro model of brain endothelial cell barrier reveals alterations induced by Plasmodium blood stage factors. Parasitol Res. 2023 Mar;122(3):729-737. doi: 10.1007/s00436-023-07782-x. Epub 2023 Jan 25. PMID: 36694092; PMCID: PMC9988999.
3. Pais TF, Ali H, Moreira da Silva J, Duarte N, Neres R, Chhatbar C, Acúrcio RC, Guedes RC, Strano Moraes MC, Costa-Silva B, Kalinke U, Penha-Gonçalves C. Brain endothelial STING1 activation by Plasmodium-sequestered heme promotes cerebral malaria via type I IFN response. Proc Natl Acad Sci U S A. 2022 Sep 6;119(36):e2206327119. doi: 10.1073/pnas.2206327119. Epub 2022 Aug 29. PMID: 36037380; PMCID: PMC9457060.
4. Pais TF, Penha-Gonçalves C. Brain Endothelium: The “Innate Immunity Response Hypothesis” in Cerebral Malaria Pathogenesis. Front Immunol. 2019 Jan 29;9:3100. doi: 10.3389/fimmu.2018.03100. PMID: 30761156; PMCID: PMC6361776.
5. Pais TF, Szegő ÉM, Marques O, Miller-Fleming L, Antas P, Guerreiro P, de Oliveira RM, Kasapoglu B, Outeiro TF. The NAD-dependent deacetylase sirtuin 2 is a suppressor of microglial activation and brain inflammation. EMBO J. 2013 Oct 2;32(19):2603-16. doi: 10.1038/emboj.2013.200. Epub 2013 Sep 6. PMID: 24013120; PMCID: PMC3791374.