CV Lattes
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Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. Escola Paulista de Medicina (EPM) (Institutional affiliation from the last research proposal) Birthplace: Brazil
Full Professor in the Department of Pharmacology at the Paulista School of Medicine (EPM), Federal University of São Paulo (UNIFESP), and mother of Caique (born March 21, 1997) and Lucca (born March 15, 2002).She earned her Bachelors degree in Biological Sciences from Instituto Mackenzie (1995), a direct PhD (19992003) and postdoctoral fellowship (20032005) in Immunology from the University of São Paulo (USP), and received her Habilitation (Livre-Docência) in Immunology from UNIFESP (2013). She completed research fellowships at the Gulbenkian Institute of Science in Portugal (2004) and Genentech Inc. in the United States (2016).At UNIFESP, she served as Vice-Head (20102011) and Head (20122013) of the Department of Biological Sciences, as well as Graduate Studies Coordinator in the Office of Graduate and Research Affairs (20172018). Within the Brazilian Society for Immunology (SBI), she has held positions as General Secretary (20162017) and Vice-President (20202021).She was Chair of the 2019 Keystone Symposium Why So Many Ways to Die and is currently a member of the Keystone Symposia Programming Consultants group.Her research focuses on innate immunity, with an emphasis on the role of inflammasomes in macrophage and astrocyte programming, and on their impact on infection control and inflammatory pathologies. (Source: Lattes Curriculum)
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The inflammasomes are multiprotein cytoplasmic complexes that play a crucial role in the immune response, activating caspase-1 and promoting the cleavage of pro-IL-1², pro-IL-18, and Gasdermin-D (GSDMD). GSDMD, by forming pores in the cell membrane, leads to the release of active forms of IL-1² and IL-18, triggering cell death through pyroptosis, which is associated with the control of in…
Several viruses have the ability to invade the Central Nervous System (CNS), infecting resident cells and causing severe neuroinflammation by activating the innate immune system. Exacerbated inflammatory responses are influenced by the activation of inflammasomes, which are multiprotein platforms present in the cytosol of different cell types capable of activating the caspase-1 protease, …
The intracellular protozoan Trypanosoma cruzi is the causative agent of Chagas disease, a serious and chronic pathology that affects millions of people worldwide. It is known that control of T. cruzi infection requires the actions of multiple mechanisms of innate immunity that are triggered by pattern recognition receptors (PRRs). Recently, our group demonstrated the involvement of NLRP3 …
(Only some records are available in English at this moment)
Inflammasomes are multiprotein cytosolic complexes whose activation results in the cleavage of the protease caspase-1, the release of interleukins IL-1b and IL-18, and cell death by pyroptosis. In the central nervous system, inflammasomes are primarily found in microglia, the main innate immune cells of the nervous system. Certain immunological stimuli, such as exposure to lipopolysacchar…
The innate immune response is based on the perception of different types of molecular patterns by pattern recognition receptors, including inflammasomes. Inflammasomes are multiprotein cytosolic complexes which, when activated, lead to the production of the active form of caspase-1, a protease whose action results in the release of interleukins (IL-)1² and IL-18 and pyroptosis. Inflammaso…
Inflammasomes are multiprotein cytoplasmic complexes capable of activating caspase-1, which in turn cleaves pro-IL-1 beta, pro-IL-18 and Gasdermin-D (GDSMD). GSDMD is able to form pores in the cell membrane resulting in the secretion of active forms of IL-1 beta and IL-18 and induction of cell death by pyroptosis. Several inflammasomes are activated during T. gondii infection, resulting i…
Inflammasomes are cytosolic multiprotein complexes activated in response to infection or cell damage. The activation of these platforms leads to recruitment and self-cleavage of the effector protease caspase-1 and consequent release of IL-1B and IL-18, and induction of a specific form of cell death, pyroptosis. These complexes are found in various immune cells such as macrophages, neutrop…
Several viruses have the ability to invade the Central Nervous System (CNS), which can infect resident cells and cause severe neuroinflammation by activating the innate immune system. It is known that these highly inflammatory processes are influenced by the activation of inflammasomes, which are multiprotein platforms present in the cytosol of different cell types, capable of activating …
(Only some records are available in English at this moment)
Inflammasomes are molecular complexes that detect sterile or infectious stimuli and trigger caspase-1 activation, leading to the release of IL-1² and IL-18 and cell death by pyroptosis. NLRP3 is assembled in response to pathogenic microorganisms and sterile signals, while NAIP/NLRC4 is classically activated by bacterial protein that reaches the cytosol, such as flagellin. In different con…
Flagellin is an agonist of TLR and NLR receptors that has been extensively investigated as an adjuvant. Innate immune recognition of flagellin is shared by transmembranic TLR5 and cytosolic Naip5/NLRC4 inflammasome complex. We have demonstrated a process of necrotic cell death induced by cytosolic flagellin that does not require NLRC4, ASC or caspase-1/11 but it is regulated by lysosomal …
The discovery of two large families of receptors that recognize a range of molecular patterns associated with pathogens, was of great importance for the understanding of recognition mechanisms mediated by innate immunity cells. These two families which include the transmembrane Toll-like receptors (TLRs) and cytoplasmic receptors, NOD-like receptors (NLRs), although induce distinct respon…
| 1 / 1 | Ongoing grants |
| 9 / 9 | Completed research grants |
| 2 / 2 | Ongoing scholarships in Brazil |
| 23 / 19 | Completed scholarships in Brazil |
| 3 / 3 | Completed scholarships abroad |
| 38 / 34 | All research grants and scholarships |
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