Keyla Sá, PhD
Postdoctoral AssociateAbout
Titles
Postdoctoral Associate
Biography
I am a Pew Latin American Fellow and postdoctoral researcher in the Department of Immunobiology at Yale School of Medicine under the guidance of Dr. Akiko Iwasaki. My work investigates how pathogenic autoantibodies emerge after infections and contribute to chronic diseases such as Long COVID and ME/CFS. I integrate large-scale proteomics, immunology, and translational approaches to uncover mechanisms of neuro-immune interactions and identify therapeutic targets. My long-term goal is to establish an independent research program focused on autoantibody-mediated neurological chronic diseases and precision medicine.
For a complete list of publications: https://scholar.google.com/cit...
Last Updated on September 25, 2025.
Education & Training
- PhD
- Universidade de São Paulo, Cellular and molecular biology (2022)
- MSc
- Universidade Federal do Pará, Biology of Infectious and Parasitic Agents (2018)
- BSc
- Universidade Federal do Pará, Biomedicine (2016)
Research
Publications
2026
A causal link between autoantibodies and neurological symptoms in long COVID
de Sá K, Silva J, Bayarri-Olmos R, Baker C, Lu Z, Gipson W, Na D, Chen B, Wenxue L, Khosroabadi D, Brinda R, Constable R, Omene B, Colom Díaz P, Kwon D, Rodrigues G, Heidecke H, Schulze-Forster K, Gross A, Shneer T, Clarke A, Linnekin T, Brate A, Brown L, Buda H, Jatiani S, Moise L, Greene K, Bhagchandani S, Bhattacharjee B, Gehlhausen J, Wood J, Tabacof L, Scheibenbogen C, Liu Y, Guan L, Schneeberger Pane M, Putrino D, Horvath T, Iwasaki A. A causal link between autoantibodies and neurological symptoms in long COVID. Cell 2026, 189: 3214-3235.e37. PMID: 42208499, DOI: 10.1016/j.cell.2026.04.042.Peer-Reviewed Original ResearchConceptsCentral nervous systemNeurological symptomsPatient's symptomsPain-related neuronal activityPassive transferAcute SARS-CoV-2 infectionAntibody-dependent phagocytosisTissue-based immunofluorescenceSARS-CoV-2 infectionPurified immunoglobulin GHuman locus coeruleusThermal hyperalgesiaFunctional autoantibodiesFatigue-like behaviorMass spectrometry assayMouse sciatic nerveTransfer of IgGAdrenal glandNerve damageLocus coeruleusPathogenic roleAutoantibodiesPassive transfer of IgGSciatic nerveAutoantibody targets
2025
SARS-CoV‑2 Aerosol Susceptibility to Bipolar Ion Disinfection
Angel D, Luhung I, de Sá K, Peccia J. SARS-CoV‑2 Aerosol Susceptibility to Bipolar Ion Disinfection. ACS ES&T Air 2025, 2: 3054-3060. DOI: 10.1021/acsestair.5c00313.Peer-Reviewed Original ResearchThe Susceptibility of Airborne SARS-CoV‑2 to Far-UVC Irradiation
Angel D, Luhung I, de Sá K, Peccia J. The Susceptibility of Airborne SARS-CoV‑2 to Far-UVC Irradiation. Environmental Science And Technology 2025, 59: 20526-20535. PMID: 40970481, DOI: 10.1021/acs.est.5c09275.Peer-Reviewed Original ResearchMucosal unadjuvanted booster vaccines elicit local IgA responses by conversion of pre-existing immunity in mice
Kwon D, Mao T, Israelow B, Santos Guedes de Sá K, Dong H, Iwasaki A. Mucosal unadjuvanted booster vaccines elicit local IgA responses by conversion of pre-existing immunity in mice. Nature Immunology 2025, 26: 908-919. PMID: 40360777, PMCID: PMC12133566, DOI: 10.1038/s41590-025-02156-0.Peer-Reviewed Original ResearchMucosal immunityIgA responsesMemory CD4+ T cellsInduce robust mucosal immunitySARS-CoV-2 spike proteinCD4+ T cellsLocal protective immune responseRobust mucosal immunityRespiratory tractMRNA-LNP vaccinesIgA-secreting plasma cellsB cell recruitmentInduce mucosal immunityPre-existing immunityProtective immune responsesLower respiratory tractRecombinant SARS-CoV-2 spike proteinLocal IgA responseIntranasal boosterMucosal boostingIntranasal boostSpike proteinMRNA-LNPChemokines CXCL9T cells
2024
Pulmonary inflammation and viral replication define distinct clinical outcomes in fatal cases of COVID-19
de Sá K, Amaral L, Rodrigues T, Caetano C, Becerra A, Batah S, Lopes F, de Oliveira I, Lopes L, Almeida L, Mota C, Oliveira S, Wada D, Koenigkam-Santos M, Martins R, Rosales R, Arruda E, Fabro A, Zamboni D. Pulmonary inflammation and viral replication define distinct clinical outcomes in fatal cases of COVID-19. PLOS Pathogens 2024, 20: e1012222. PMID: 38838044, PMCID: PMC11182505, DOI: 10.1371/journal.ppat.1012222.Peer-Reviewed Original ResearchConceptsViral loadClinical outcomesCOVID-19 patientsPulmonary inflammationInflammatory profileLethal casesInflammasome activationFatal casesViral replicationFatal cases of COVID-19Mechanical ventilation timeSARS-CoV-2NLRP3-/- miceSevere COVID-19Robust inflammasome activationCases of COVID-19Immune-mediatedVentilation timeLittermate micePulmonary fibrosisDisease exacerbationPathophysiological mechanismsTransgenic miceHistopathological statusNLRP3-/-Alpha 1-acid glycoprotein is upregulated in severe COVID-19 patients and decreases neutrophil NETs in SARS-CoV-2 infection
Mestriner F, Francisco D, Campos L, Couto A, Fraga-Silva T, Flora Dugaich V, D Avila-Mesquita C, Zukowski Kovacs H, Vasconcelos J, Milani E, Santos Guedes de Sá K, Martins R, Jordani M, Corsi C, Barbosa J, Vasconcelos T, Gonçalves Menegueti M, Neto J, da Costa R, Evora P, Arruda E, Tostes R, Polonis K, Bonato V, Auxiliadora-Martins M, Ribeiro M, Becari C. Alpha 1-acid glycoprotein is upregulated in severe COVID-19 patients and decreases neutrophil NETs in SARS-CoV-2 infection. Cytokine 2024, 176: 156503. PMID: 38301358, DOI: 10.1016/j.cyto.2024.156503.Peer-Reviewed Original ResearchConceptsAlpha 1-acid glycoprotein levelsSevere COVID-19 patientsAlpha 1-acid glycoproteinSARS-CoV-2 infectionIL-6COVID-19 patientsSARS-CoV-2Blood samplesC-reactive proteinIL-6 productionLaboratory parametersCOVID-19 infected patientsAcute-phase proteinsCOVID-19 infectionSevere acute respiratory syndrome coronavirus 2Acute respiratory syndrome coronavirus 2Infected patientsRespiratory syndrome coronavirus 2Inhibitor of neutrophil migrationCytokine stormImmunomodulating effectsFlow cytometrySystem injurySyndrome coronavirus 2Patients
2023
Gasdermin-D activation promotes NLRP3 activation and host resistance to Leishmania infection
de Sá K, Amaral L, Rodrigues T, Ishimoto A, de Andrade W, de Almeida L, Freitas-Castro F, Batah S, Oliveira S, Pastorello M, Fabro A, Zamboni D. Gasdermin-D activation promotes NLRP3 activation and host resistance to Leishmania infection. Nature Communications 2023, 14: 1049. PMID: 36828815, PMCID: PMC9958042, DOI: 10.1038/s41467-023-36626-6.Peer-Reviewed Original ResearchConceptsGasdermin DKDa fragmentFunction of gasdermin-DInflammasome activationNLRP3 inflammasome activationGasdermin D activationCell permeabilizationSkin biopsiesNLRP3 inflammasomeMolecular mechanismsHost resistanceNormal functionIntracellular parasitesSkin biopsies of patientsActivate NLRP3 inflammasomeLeishmania genusBiopsies of patientsLeishmania speciesLeishmania infectionResistance to Leishmania infectionSusceptibility to infectionTransient cell permeabilizationNLRP3 activationInflammasomeNLRP3CASP4/11 Contributes to NLRP3 Activation and COVID-19 Exacerbation
Rodrigues T, Caetano C, de Sá K, Almeida L, Becerra A, Gonçalves A, de Sousa Lopes L, Oliveira S, Mascarenhas D, Batah S, Silva B, Gomes G, Castro R, Martins R, Avila J, Frantz F, Cunha T, Arruda E, Cunha F, Nakaya H, Cunha L, Fabro A, Louzada-Junior P, de Oliveira R, Zamboni D. CASP4/11 Contributes to NLRP3 Activation and COVID-19 Exacerbation. Journal Of Infectious Diseases 2023, 227: 1364-1375. PMID: 36763010, DOI: 10.1093/infdis/jiad037.Peer-Reviewed Original ResearchConceptsFatal casesNLRP3 activationFatal cases of COVID-19Expression of inflammasome componentsSevere COVID-19In vivo infectionHumanized miceSevere acute respiratory syndrome coronavirus 2Acute respiratory syndrome coronavirus 2COVID-19 exacerbationClinical scoresInflammatory mediatorsRespiratory syndrome coronavirus 2Parenchymal areaSyndrome coronavirus 2Patient's lungsTherapeutic interventionsSARS-CoV-2Inflammasome componentsMiceNLRP3 inflammasomeNLRP3DiseaseCoronavirus 2COVID-19
2022
Ativação do inflamassoma: a importância na leishmaniose, na influenza e na COVID-19
de Sá K. Ativação do inflamassoma: a importância na leishmaniose, na influenza e na COVID-19. 2022 DOI: 10.11606/t.17.2022.tde-03022023-110423.Peer-Reviewed Original ResearchIdentification of immunomodulatory drugs that inhibit multiple inflammasomes and impair SARS-CoV-2 infection
de Almeida L, da Silva A, Rodrigues T, Oliveira S, Ishimoto A, Seribelli A, Becerra A, Andrade W, Ataide M, Caetano C, de Sá K, Pelisson N, Martins R, de Paula Souza J, Arruda E, Batah S, Castro R, Frantz F, Cunha F, Cunha T, Fabro A, Cunha L, Louzada-Junior P, de Oliveira R, Zamboni D. Identification of immunomodulatory drugs that inhibit multiple inflammasomes and impair SARS-CoV-2 infection. Science Advances 2022, 8: eabo5400. PMID: 36103544, PMCID: PMC9473568, DOI: 10.1126/sciadv.abo5400.Peer-Reviewed Original ResearchConceptsSmall-molecule compound libraryCompound librariesHigh-throughput screeningInduction of autophagySARS-CoV-2 infectionFDA-approved drugsSARS-CoV-2Mouse modelMouse model of SARS-CoV-2 infectionModel of SARS-CoV-2 infectionExcessive inflammatory processInflammasome activationAsymptomatic COVID-19Inhibition of NLRP3Immunomodulatory drugsSevere acute respiratory syndrome coronavirus 2Acute respiratory syndrome coronavirus 2Respiratory syndrome coronavirus 2NAIP/NLRC4 inflammasomeInflammatory processDisease aggravationImmunomodulatory functionsCOVID-19 treatmentHuman monocytesSyndrome coronavirus 2
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