Ioanna Evdokia Galani

@bioacademy.gr

Center for Basic Research
Biomedical Research Foundation of the Academy of Athens (BRFAA)

Ioanna Evdokia Galani


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https://researchid.co/igalani

RESEARCH, TEACHING, or OTHER INTERESTS

Immunology
35

Scopus Publications

Scopus Publications

  • Polyunsaturated fatty acid-derived lipid mediator patterns determine viral pneumonia severity and risk for critical COVID-19
    Maria Papadaki, Eleftherios Pavlos, Marc Dubourdeau, Vincent Bailif, Kamal Badirou, Clémence A. Gély, Ioanna-Evdokia Galani, Dimitris Papelis, Natalia Kamperi, Vasiliki Triantafyllia, Eleni Siouti, Maria Salagianni, Maria Manioudaki, Nikolaos Paschalidis, Giannis Vatsellas, Evangelia Koukaki, Vasiliki Rapti, Dimitris Thanos, Nikoletta Rovina, Garyfallia Poulakou, Aurélie Cobat, Jean-Laurent Casanova, Constantin Tamvakopoulos, Evangelos Andreakos
    Proceedings of the National Academy of Sciences of the United States of America, 2026
    Severe respiratory infections such as COVID-19 are characterized by excessive inflammation leading to the development of pneumonia and acute respiratory distress syndrome. Bioactive lipid mediators (LMs) derived from ω6 and ω3 polyunsaturated fatty acids are central to the regulation of inflammation, controlling both its initiation and resolution. Still, their role in viral infections remains underexplored. By employing a holistic approach involving the analysis of white blood cell transcriptomes, targeted lipidomics, cytokine and immune cell profiling, we now show that LM patterns around hospital admission are profoundly altered in COVID-19, correlate with inflammatory responses, and stratify patients according to disease severity. Central to this are CYP450-derived LMs, such as 20-HETE, and lipoxygenase- or nonenzymatic-associated LMs such as 15-HETE, both exhibiting vasoactive function, along with lipid peroxidation metabolites such as 10-HDOHE. Among them, increased 20-HETE appears to be a promising prognostic biomarker for ICU admission and a potential therapeutic target for severe COVID-19 disease. Our study emphasizes the importance of LM patterns in COVID-19 pathophysiology and sheds light into the broader immune mechanisms beyond cytokines driving viral pneumonia in humans.
  • In-Treatment Kinetics of Peripheral Blood Immune Markers in PD-L1 High Non-Small Cell Lung Cancer and Prognostic Relevance for Immunotherapy Outcomes
    Ioannis P. Trontzas, Ioanna-Evdokia Galani, Emmanouil Panagiotou, Efthymia Theofani, Anastasia Georganta, Konstantinos G. Kyriakoulis, Anastasia Palaiologou, Ioannis Vathiotis, Constantin Tamvakopoulos, Evangelos Andreakos, Konstantinos N. Syrigos
    Cancers, 2026
    Background: A substantial proportion of patients with non-small cell lung cancer (NSCLC) derive limited clinical benefit from immunotherapy. Monitoring of peripheral blood immune markers (PBIMs) may emerge as a useful tool to predict treatment outcomes with immune checkpoint inhibitors (ICIs). Patients/Methods: We prospectively measured several PBIMs in a PD-L1 high (TPS ≥ 50%) NSCLC cohort of patients treated with first-line pembrolizumab monotherapy. Kinetics over the first year of treatment were assessed at baseline (T0) and at 21 days (T1), 3 months (T2), 6 months (T3) and at 1 year (T4) post-treatment initiation. Associations with clinical outcomes were explored after a 2-year follow-up period. Results: In total, 31 patients with PD-L1 high locally advanced or metastatic NSCLC were prospectively enrolled. Over the first year of treatment, levels of CRP, IL-17α, IL-6, and IL-8 were significantly decreased. Early kinetics analysis showed significant decrease in total leukocytes, neutrophils, CRP, and MIP-3α/CCL20, as well as significant transient elevation of ITAC/CXCL11, IL-1β, IL-7, and TNFα, during the first 3 months of treatment. Early percent changes (Δ% at T1 and at T2) of ‘low’ vs. ‘high’ pretreatment levels showed significant differences for LDH, ITAC/CXCL11, GM-CSF, MIP-1α/CCL3, IL-2, IL-4, IL-5, and sPD-L1. Longitudinal analysis, stratified per responders and for pre-progression fluctuations, did not reveal significant findings. Among markers with acceptable discriminative performance, higher baseline CRP, complement C4, and IL-6 levels were associated with poorer clinical outcomes. In multivariable analysis, only C4 retained independent prognostic significance; however, integration of these PBIMs into composite indices improved prognostic performance. Conclusions: In this prospective study, longitudinal monitoring of PBIMs provided descriptive insights into immune and inflammatory dynamics during pembrolizumab treatment; however, no significant associations were observed between in-treatment biomarker kinetics and clinical outcomes. In exploratory analyses, baseline CRP, complement C4, and IL-6 levels were associated with clinical outcomes, and their integration into composite indices improved prognostic performance. These findings suggest that specific baseline PBIMs may carry prognostic relevance, while the role of in-treatment monitoring remains to be further clarified in larger prospective studies.
  • Proceedings of the 2nd Symposium "Autoimmune Diseases - Clinical Unmet Needs in Systemic Autoimmune Diseases Guide Clinical, Translational, and Basic Research&quot
    Loukas Chatzis, Ioanna Myrto Theofani, Ioanna E. Galani, Panagiota Palla, Alexandra Koutsogianni, et al.
    Mediterranean Journal of Rheumatology, 2026
  • Transcriptomic analysis reveals shared deregulated neutrophil responses in COVID-19 and idiopathic pulmonary fibrosis
    Georgios Divolis, Evgenia Synolaki, Rodoula Tringidou, Argyrios Tzouvelekis, Dimitrios T. Boumpas, Panagiotis Skendros, Ioanna-Evdokia Galani
    Respiratory Research, 2025
    BACKGROUND: Coronavirus disease 2019 (COVID-19) is a respiratory disease linked with deregulated immune responses, leading to hyperinflammation, acute respiratory distress syndrome, and pulmonary fibrosis, often with fatal outcomes. Neutrophils play a central role in COVID-19 pathogenesis, with elevated peripheral blood neutrophil counts correlating with disease severity. Despite extensive research, the molecular processes associated with neutrophil hyperactivation in COVID-19 remain elusive. METHODS: To investigate the molecular signatures underlying neutrophil-driven pathology, we conducted transcriptome analysis in neutrophils isolated from the peripheral blood of COVID-19 patients versus healthy individuals. To evaluate the specificity of identified neutrophil signatures in COVID-19, we extended our transcriptomic analysis to neutrophils from patients with idiopathic pulmonary fibrosis (IPF), a non-infectious fibrotic lung disease. Additionally, immunofluorescence staining was performed on lung biopsy specimens from IPF patients to validate transcriptomic findings at the tissue level. RESULTS: Our analysis revealed significant transcriptional changes in COVID-19 neutrophils, particularly in pathways involved in immune regulation, inflammation, and antiviral responses. Additionally, pathways associated with autophagy and chromatin remodeling were upregulated, while translation-related processes were suppressed, indicating an increased predisposition for neutrophil extracellular trap (NET) release. This neutrophil transcriptional signature in COVID-19 appears to be associated with the previously reported deregulation of the Activin/Follistatin system in the periphery. Notably, a comparative transcriptomic analysis with neutrophils isolated from IPF patients revealed the induction of substantially overlapping inflammatory processes, suggesting common deregulated responses in COVID-19 and IPF. Consistently, significant NET formation, a hallmark of COVID-19-related inflammation, was observed within lung biopsies from IPF patients. CONCLUSION: By delineating both shared and disease-specific molecular pathways, our findings validate the critical role of neutrophils in COVID-19 and IPF pathophysiology, highlighting their involvement in balancing the inflammatory response across diverse lung diseases.
  • CD40-CD40L inhibition attenuates platelet-neutrophil interaction and neutrophil extracellular trap release in primary antiphospholipid syndrome
    Stavros Naoum, Charilaos Spyropoulos, Andriani Angelopoulou, Harikleia Gakiopoulou, Michalis Katsimpoulas, Vassilis G. Gorgoulis, Petros P. Sfikakis, Konstantinos Ritis, Ioanna-Evdokia Galani, Konstantinos Kambas, Maria G. Tektonidou
    Annals of the Rheumatic Diseases, 2025
    OBJECTIVES: Neutrophil extracellular traps (NETs) are increasingly recognised for their role in primary antiphospholipid syndrome (PAPS) pathogenesis. Herein, we examined underlying mechanisms driving NET formation and the thrombogenic effects of NETs in patients with PAPS, along with potential inhibitors. METHODS: We examined NET release in PAPS, asymptomatic antiphospholipid autoantibodies (aPLs) carriers, and healthy controls (HCs) as well as NET-bound proteins by immunofluorescence, immunoblotting, quantitative polymerase chain reaction (PCR), and enzyme-linked immunosorbent assay (ELISA). We assessed platelet-neutrophil aggregates by flow cytometry (CD61/CD66b staining) and autophagy using LC3B immunofluorescence and immunoblotting. Immunofluorescence was performed in paraffin-embedded kidney, skin ulcer, and endoarterial thrombus tissues from patients with PAPS. Suppression of NET release via CD40-CD40L inhibition was tested in in vitro and venous thrombosis mouse models. RESULTS: Neutrophils from patients with PAPS exhibited increased NET release compared with asymptomatic aPL carriers and HCs. NETs from patients with PAPS expressed tissue factor (TF) that induced thrombin generation in platelet-poor plasma from HCs. aPL induced in vitro intracellular TF expression in HC neutrophils. TF-expressing NETs were abundant in the kidney, skin ulcer, and endoarterial thrombus tissues from patients with PAPS, and colocalised with fibrinogen. NET release in PAPS neutrophils was driven by aPL-mediated platelet activation, subsequent platelet-neutrophil interaction, and autophagy induction. CD40-CD40L blockade reduced platelet activation, autophagy, and NET formation in patients with PAPS. In a mouse model, inhibition of CD40-CD40L reduced neutrophil-platelet aggregates and myeloperoxidase (MPO)-DNA complexes in mouse peripheral blood, and the presence of NETs in the formed thrombi. CONCLUSIONS: Targeting the platelet-neutrophil/autophagy/TF-expressing NETs axis by CD40-CD40L inhibition attenuates thromboinflammation in PAPS and should be explored as a potential therapeutic target.
  • Multiparametric analysis in the peripheral blood of Giant Cell Arteritis and Polymyalgia Rheumatica patients at the early phases of steroid treatment reveals changes in cell subpopulations and lipid mediators: a preliminary study
    Dimitris Anastasios Palamidas, Maria Papadaki, Nikolaos Paschalidis, Eleftherios Pavlos, Loukas Chatzis, Panagiota Palla, Ourania D. Argyropoulou, Dionysios Prevezanos, Marc Dubourdeau, Konstantinos Kambas, Ioanna Evdokia Galani, Andreas V. Goules, Evangelos Andreakos, Athanasios G. Tzioufas
    Frontiers in Immunology, 2025
    IntroductionGiant Cell Arteritis (GCA) and Polymyalgia Rheumatica (PMR) are autoimmune/autoinflammatory disorders presenting as acute inflammatory responses and are highly responsive to steroids. In this report, we aim to decipher the immune landscape including immune cell subpopulations, plasma cytokines, and small lipid mediators (LMs) at the very early stages of steroid treatment initiation in 4 distinct time points at: 0h (T1), 48h (T2), 96h (T3), and 24 weeks (T4).Patients and methodsSerum, plasma and peripheral blood mononuclear cells (PBMCs) were collected prospectively from 8 GCA and 6 PMR newly diagnosed patients. Sixteen healthy individuals served as controls (HC). Deep immunophenotyping by CyTOF was performed in PBMCs at T1-T3. A multiplex Luminex assay measured serum levels of 21 cytokines at T1 and T3. Levels of lipid mediators (LMs) were evaluated at T1, T3 and T4 with the LC-MS/MS method.ResultsTotal CD8+ T cells and DCs were decreased within 48–96 hours, following steroid treatment, while B-cells were increased at 48 hours. Further analysis of immune subpopulations containing the major cell types revealed different frequencies of distinct CD8+, CD4+, DCs, and B cell subtypes. Out of 21 cytokines/chemokines evaluated, only ITAC levels were decreased at T3. The ratio of pro/anti-inflammatory LMs was high at T1 in patients with either PMR or GCA. However, 6 months after steroid treatment it returned to normal in PMR patients, but remained high in GCA patients, providing the only discriminatory element between the two diseases.ConclusionThe rapid clinical improvement of GCA and PMR patients, following steroid treatment, is associated with immune cell type alterations, but it is poorly associated with plasma cytokine levels. Small lipid mediators can differentiate GCA and PMR patients. The persistently elevated levels of pro-inflammatory LMs might be related to the underlying residual tissue inflammation described in GCA. These preliminary results suggest that further studies in a larger patient cohort are required to validate these findings.
  • Exploring the Impact of Airway Microbiome on Asthma Morbidity: A Focus on the “Constructing a ‘Eubiosis Reinstatement Therapy’ for Asthma—CURE” Project
    Paraskevi Xepapadaki, Spyridon Megremis, Nikoletta Rovina, Aleksandra Wardzyńska, Maria Pasioti, Maria Kritikou, Nikolaos G. Papadopoulos, , Grigoris Kaltsas, Evangelia Lebessi, Anastassios Doudoulakakis, Stella Taka, Panagiota Tzani Tzanopoulou, Evangelia Legaki, Rena Stergiou, David Robertson, Tucker Gilman, Mark Muldoon, Avraam Tapinos, Chuan Fu Yap, George Gkimpas, Joe Busby, Mubeccel Akdis, Cezmi Akdis, Anna Globinska, Ramazan Rozumbetov, Vangelis Andreakos, Ioanna Galani, Mikaela Koutrouli, Vaso Triantafullia, Hannah Wanstall, Maria Papadaki, Marek† Kowalski, Aleksandra Wardzyńska, Maciej Chałubiński, Nina Chanishvili, Elene Kakabadze, Marina Goderdzishvili, Valeria Ramiconi, Isabel Proano, Sofia Romagosa, Christos Ilioudis, Athina Thanopoulou, Dimitris Raptis
    Pulmonary Therapy, 2024
    The asthma pandemic imposes a huge burden on patients and health systems in both developed and developing countries. Despite available treatments, symptom control is generally suboptimal, and hospitalizations and deaths remain at unacceptably high levels. A pivotal aspect of asthma that warrants further exploration is the influence of the respiratory microbiome and virome in modulating disease activity. A plethora of studies report that the respiratory microbiome is characteristically dysbiotic in asthma. In addition, our data suggest that dysbiosis is also observed on the respiratory virome, partly characterized by the reduced abundance of bacteriophages (phages). Even though phages can naturally infect and control their bacterial prey, phage therapy has been grossly neglected in the Western world, although more recently it is more widely used as a novel tool against bacterial infections. However, it has never been used for tackling microbiome dysbiosis in human non-communicable diseases. This review provides an up-to-date understanding of the microbiome and virome's role within the airways in relation to asthma morbidity. It also advances the rationale and hypothesis for the CURE project. Specifically, the CURE project suggests that managing the respiratory microbiome through phage therapy is viable and may result in restoring eubiosis within the asthmatic airway. This entails controlling immune dysregulation and the clinical manifestation of the disease. To accomplish this goal, it is crucial to predict the effects of introducing specific phage mixtures into the intricate ecology of the airways and devise suitable interventions.
  • Notch signaling in adipose tissue macrophages prevents diet-induced inflammation and metabolic dysregulation
    Eleni Siouti, Maria Salagianni, Maria Manioudaki, Eleftherios Pavlos, Apostolos Klinakis, Ioanna‐Evdokia Galani, Evangelos Andreakos
    European Journal of Immunology, 2024
    The importance of macrophages in adipose tissue (AT) homeostasis and inflammation is well established. However, the potential cues that regulate their function remain incompletely understood. To bridge this important gap, we sought to characterize novel pathways involved using a mouse model of diet‐induced obesity. By performing transcriptomics analysis of AT macrophages (ATMs), we found that late‐stage ATMs from high‐fat diet mice presented with perturbed Notch signaling accompanied by robust proinflammatory and metabolic changes. To explore the hypothesis that the deregulated Notch pathway contributes to the development of AT inflammation and diet‐induced obesity, we employed a genetic approach to abrogate myeloid Notch1 and Notch2 receptors. Our results revealed that the combined loss of Notch1 and Notch2 worsened obesity‐related metabolic dysregulation. Body and AT weight gain was higher, blood glucose levels increased and metabolic parameters were substantially worsened in deficient mice fed high‐fat diet. Moreover, serum insulin and leptin were elevated as were triglycerides. Molecular analysis of ATMs showed that deletion of Notch receptors escalated inflammation through the induction of an M1‐like pro‐inflammatory phenotype. Our findings thus support a protective role of myeloid Notch signaling in adipose tissue inflammation and metabolic dysregulation.
  • Type III interferons in innate and adaptive immunity in the respiratory tract
    Artemios Piperakis, Ioanna E Galani, Evangelos Andreakos
    Current Opinion in Immunology, 2024
  • Comprehensive Analysis of 1-Year-Old Female Apolipoprotein E-Deficient Mice Reveals Advanced Atherosclerosis with Vulnerable Plaque Characteristics
    Sotirios Kotsovilis, Maria Salagianni, Aimilia Varela, Constantinos H. Davos, Ioanna E. Galani, Evangelos Andreakos
    International Journal of Molecular Sciences, 2024
    Apolipoprotein E-knockout (Apoe-/-) mice constitute the most widely employed animal model of atherosclerosis. Deletion of Apoe induces profound hypercholesterolemia and promotes the development of atherosclerosis. However, despite its widespread use, the Apoe-/- mouse model remains incompletely characterized, especially at late time points and advanced disease stages. Thus, it is unclear how late atherosclerotic plaques compare to earlier ones in terms of lipid deposition, calcification, macrophage accumulation, smooth muscle cell presence, or plaque necrosis. Additionally, it is unknown how cardiac function and hemodynamic parameters are affected at late disease stages. Here, we used a comprehensive analysis based on histology, fluorescence microscopy, and Doppler ultrasonography to show that in normal chow diet-fed Apoe-/- mice, atherosclerotic lesions at the level of the aortic valve evolve from a more cellular macrophage-rich phenotype at 26 weeks to an acellular, lipid-rich, and more necrotic phenotype at 52 weeks of age, also marked by enhanced lipid deposition and calcification. Coronary artery atherosclerotic lesions are sparse at 26 weeks but ubiquitous and extensive at 52 weeks; yet, left ventricular function was not significantly affected. These findings demonstrate that atherosclerosis in Apoe-/- mice is a highly dynamic process, with atherosclerotic plaques evolving over time. At late disease stages, histopathological characteristics of increased plaque vulnerability predominate in combination with frequent and extensive coronary artery lesions, which nevertheless may not necessarily result in impaired cardiac function.
  • Neutrophil-derived Activin-A moderates their pro-NETotic activity and attenuates collateral tissue damage caused by Influenza A virus infection
    Georgios Divolis, Evgenia Synolaki, Athanasia Doulou, Ariana Gavriil, Christina C. Giannouli, Anastasia Apostolidou, Martyn L. Foster, Martin M. Matzuk, Panagiotis Skendros, Ioanna-Evdokia Galani, Paschalis Sideras
    Frontiers in Immunology, 2024
  • Autoantibodies against type I IFNs in patients with critical influenza pneumonia
    Qian Zhang, Andrés Pizzorno, Lisa Miorin, Paul Bastard, Adrian Gervais, Tom Le Voyer, Lucy Bizien, Jeremy Manry, Jérémie Rosain, Quentin Philippot, Kelian Goavec, Blandine Padey, Anastasija Cupic, Emilie Laurent, Kahina Saker, Martti Vanker, Karita Särekannu, , Laurent Abel, Alessandro Aiuti, Saleh Al-Muhsen, Fahd Al-Mulla, Mark S. Anderson, Evangelos Andreakos, Andrés A. Arias, Hagit Baris Feldman, Alexandre Belot, Catherine M. Biggs, Dusan Bogunovic, Alexandre Bolze, Anastasiia Bondarenko, Ahmed A. Bousfiha, Petter Brodin, Yenan Bryceson, Carlos D. Bustamante, Manish J. Butte, Giorgio Casari, John Christodoulou, Antonio Condino-Neto, Stefan N. Constantinescu, Megan A. Cooper, Clifton L. Dalgard, Murkesh Desai, Beth A. Drolet, Jamila El Baghdadi, Sara Espinosa-Padilla, Jacques Fellay, Carlos Flores, Paraskevi C. Fragkou, José Luis Franco, Antoine Froidure, Ioanna Evdokia Galani, Peter K. Gregersen, Bodo Grimbacher, Filomeen Haerynck, David Hagin, Rabih Halwani, Lennart Hammarström, James R. Heath, Sarah E. Henrickson, Elena W.Y. Hsieh, Eystein Husebye, Kohsuke Imai, Yuval Itan, Erich D. Jarvis, Timokratis Karamitros, Kai Kisand, Ourania Koltsida, Cheng-Lung Ku, Yu-Lung Lau, Yun Ling, Carrie L. Lucas, Tom Maniatis, Davood Mansouri, László Maródi, Isabelle Meyts, Joshua D. Milner, Kristina Mironska, Trine H. Mogensen, Tomohiro Morio, Lisa F.P. Ng, Luigi D. Notarangelo, Antonio Novelli, Giuseppe Novelli, Cliona O'Farrelly, Satoshi Okada, Keisuke Okamoto, Tayfun Ozcelik, Qiang Pan-Hammarström, Jean W. Pape, Rebeca Perez de Diego, David S. Perlin, Graziano Pesole, Anna M. Planas, Carolina Prando, Aurora Pujol, Lluis Quintana-Murci, Sathishkumar Ramaswamy, Vasiliki Rapti, Laurent Renia, Igor Resnick, Carlos Rodríguez-Gallego, Nikoletta Rovina, Vanessa Sancho-Shimizu, Anna Sediva, Mikko R.J. Seppänen, Mohammed Shahrooei, Anna Shcherbina, Ondrej Slaby, Andrew L. Snow, Pere Soler-Palacín, András N. Spaan, Ivan Tancevski, Stuart G. Tangye, Ahmad Abou Tayoun, Şehime Gülsün Temel, Sotirios Tsiodras, Stuart E. Turvey, K.M. Furkan Uddin, Mohammed J. Uddin, Diederik van de Beek, Donald C. Vinh, Horst von Bernuth, Joost Wauters, Mayana Zatz, Pawel Zawadzki, Helen C. Su, Jean-Laurent Casanova, , Pascal Morel, Pascale Richard, Brigitte Bonneaudeau, Dorothée Cannet, Pierre Gallian, Michel Jeanne, Magali Perroquin, Hind Hamzeh-Cognasse, Fabrice Cognasse, Pierre Tiberghien, , Rachel Nadif, Marcel Goldberg, Anna Ozguler, Joseph Henny, Sylvie Lemonnier, Mireille Coeuret-Pellicer, Stéphane Le Got, Marie Zins, , Christophe Tzourio, Stéphanie Debette, Carole Dufouil, Aïcha Soumaré, Morgane Lachaize, Nathalie Fievet, Amandine Flaig, , Fernando Martin, Souad Mehlal-Sedkaoui, Jérôme Sallette, , Romain Hernu, Bruno Lina, Carole Schwebel, Isabelle Wroblewski, Patrice Morand, Bertrand Souweine, Benoit Boeuf, Helene Peigue-Lafeuille, Michael Darmon, Hugues Patural, Bruno Pozzetto, Jean Pierre Quenot, Benoit Colomb, Pierre Pothier, Alexandre Belot, , Maria Abad Arranz, Manuela Aguilar Guisado, Ana Escoresca Ortega, Rafaela Gallardo Ríos, Laura Merino Díaz, Maria Del Mar Muñoz Garcia, Nieves Ramírez Duque, Gloria María Romero Vázquez, Maria Jose Sánchez Cordero, Celia Salamanca Rivera, Jordi Niubó, Alexander Rombauts, Nicolás Navarrete, Laura Romero Oraa, Virginia Palomo, Tamara García-Salum, Marcela Ferres, Nicole Le Corre, Javier Sánchez-Céspedes, María Balsera-Manzanero, Jordi Carratala, Pilar Retamar-Gentil, Gabriela Abelenda-Alonso, Adoración Valiente, Pierre Tiberghien, Marie Zins, Stéphanie Debette, Isabelle Meyts, Filomeen Haerynck, Riccardo Castagnoli, Luigi D. Notarangelo, Luis I. Gonzalez-Granado, Nerea Dominguez-Pinilla, Evangelos Andreakos, Vasiliki Triantafyllia, Carlos Rodríguez-Gallego, Jordi Solé-Violán, José Juan Ruiz-Hernandez, Felipe Rodríguez de Castro, José Ferreres, Marisa Briones, Joost Wauters, Lore Vanderbeke, Simon Feys, Chen-Yen Kuo, Wei-Te Lei, Cheng-Lung Ku, Galit Tal, Amos Etzioni, Suhair Hanna, Thomas Fournet, Jean-Sebastien Casalegno, Gregory Queromes, Laurent Argaud, Etienne Javouhey, Manuel Rosa-Calatrava, Elisa Cordero, Teresa Aydillo, Rafael A. Medina, Kai Kisand, Anne Puel, Emmanuelle Jouanguy, Laurent Abel, Aurélie Cobat, Sophie Trouillet-Assant, Adolfo García-Sastre, Jean-Laurent Casanova
    Journal of Experimental Medicine, 2022
  • TFEB signaling attenuates NLRP3-driven inflammatory responses in severe asthma
    Efthymia Theofani, Maria Semitekolou, Konstantinos Samitas, Annie Mais, Ioanna E. Galani, Vasiliki Triantafyllia, Joanna Lama, Ioannis Morianos, Athanasios Stavropoulos, Se‐Jin Jeong, Evangelos Andreakos, Babak Razani, Nikoletta Rovina, Georgina Xanthou
    Allergy European Journal of Allergy and Clinical Immunology, 2022
  • Severity of neonatal influenza infection is driven by type I interferon and oxidative stress
    Ogan K. Kumova, Ioanna-Evdokia Galani, Abhishek Rao, Hannah Johnson, Vasiliki Triantafyllia, Stephanie M. Matt, Judy Pascasio, Peter J. Gaskill, Evangelos Andreakos, Peter D. Katsikis, Alison J. Carey
    Mucosal Immunology, 2022
  • CD103 integrin identifies a high IL-10-producing FoxP3+ regulatory T-cell population suppressing allergic airway inflammation
    Sofia Tagkareli, Maria Salagianni, Ioanna‐Evdokia Galani, Maria Manioudaki, Eleftherios Pavlos, Kalliopi Thanopoulou, Evangelos Andreakos
    Allergy European Journal of Allergy and Clinical Immunology, 2022
  • Protocol for influenza A virus infection of mice and viral load determination
    Ioanna-Evdokia Galani, Vasiliki Triantafyllia, Evridiki-Evangelia Eleminiadou, Evangelos Andreakos
    STAR Protocols, 2022
  • Impaired innate antiviral defenses in COVID-19: Causes, consequences and therapeutic opportunities
    Ioanna-Evdokia Galani, Evangelos Andreakos
    Seminars in Immunology, 2021
  • Untuned antiviral immunity in COVID-19 revealed by temporal type I/III interferon patterns and flu comparison
    Ioanna-Evdokia Galani, Nikoletta Rovina, Vicky Lampropoulou, Vasiliki Triantafyllia, Maria Manioudaki, Eleftherios Pavlos, Evangelia Koukaki, Paraskevi C. Fragkou, Vasiliki Panou, Vasiliki Rapti, Ourania Koltsida, Andreas Mentis, Nikolaos Koulouris, Sotirios Tsiodras, Antonia Koutsoukou, Evangelos Andreakos
    Nature Immunology, 2021
  • Human and translational immunology in the third millennium: progress, challenges and opportunities
    Ioanna E. Galani, Eynav Klechevsky, Evangelos Andreakos
    Nature Immunology, 2019
  • Lambda interferons come to light: dual function cytokines mediating antiviral immunity and damage control
    Evangelos Andreakos, Ivan Zanoni, Ioanna E Galani
    Current Opinion in Immunology, 2019
  • Interferon-λs: Front-line guardians of immunity and homeostasis in the respiratory tract
    Evangelos Andreakos, Maria Salagianni, Ioanna E. Galani, Ourania Koltsida
    Frontiers in Immunology, 2017
  • Interferon lambda1/IL-29 and inorganic polyphosphate are novel regulators of neutrophil-driven thromboinflammation
    Akrivi Chrysanthopoulou, Konstantinos Kambas, Dimitrios Stakos, Ioannis Mitroulis, Alexandros Mitsios, Veroniki Vidali, Iliana Angelidou, Magdalena Bochenek, Stella Arelaki, Athanasios Arampatzioglou, Ioanna-Evdokia Galani, Panagiotis Skendros, Elias A Couladouros, Stavros Konstantinides, Evangelos Andreakos, Katrin Schäfer, Konstantinos Ritis
    Journal of Pathology, 2017
  • Interferon-λ Mediates Non-redundant Front-Line Antiviral Protection against Influenza Virus Infection without Compromising Host Fitness
    Ioanna E. Galani, Vasiliki Triantafyllia, Evridiki-Evangelia Eleminiadou, Ourania Koltsida, Athanasios Stavropoulos, Maria Manioudaki, Dimitris Thanos, Sean E. Doyle, Sergei V. Kotenko, Kalliopi Thanopoulou, Evangelos Andreakos
    Immunity, 2017
  • Assessment of follicle viability using fluorescence microscopy before & after ovarian thawing
    C. Sofoudis, I Zervomanolakis, Ioanna E. Galani, V. Grigoriou, D. Botsis, et al.
    Clinical and Experimental Obstetrics and Gynecology, 2017
  • Neutrophils in viral infections: Current concepts and caveats
    I. E. Galani, E. Andreakos
    Journal of Leukocyte Biology, 2015
  • Type III interferons (IFNs): Emerging master regulators of immunity
    Ioanna E. Galani, Ourania Koltsida, Evangelos Andreakos
    Advances in Experimental Medicine and Biology, 2015
  • Reply: CXCL13 in tertiary lymphoid tissues: Sites of production are different from sites of functional localization
    Eleni Litsiou, Maria Semitekolou, Ioanna Galani, Ioannis Morianos, Aikaterini Tsoutsa, Panagiota Kara, Dimitra Rontogianni, Ion Bellenis, Maria Konstantinou, Konstantinos Potaris, Evangelos Andreakos, Paschalis Sideras, Spyros Zakynthinos, Maria Tsoumakidou
    American Journal of Respiratory and Critical Care Medicine, 2014
  • CXCL13 production in B cells via toll-like receptor/lymphotoxin receptor signaling is involved in lymphoid neogenesis in chronic obstructive pulmonary disease
    Eleni Litsiou, Maria Semitekolou, Ioanna E. Galani, Ioannis Morianos, Aikaterini Tsoutsa, Panagiota Kara, Dimitra Rontogianni, Ion Bellenis, Maria Konstantinou, Konstantinos Potaris, Evangelos Andreakos, Paschalis Sideras, Spyros Zakynthinos, Maria Tsoumakidou
    American Journal of Respiratory and Critical Care Medicine, 2013
  • Toll-like receptor 7 protects from atherosclerosis by constraining inflammatory macrophage activation
    Maria Salagianni, Ioanna E. Galani, Anna M. Lundberg, Constantinos H. Davos, Aimilia Varela, Ariana Gavriil, Leo-Pekka Lyytikäinen, Terho Lehtimäki, Fragiska Sigala, Lasse Folkersen, Vassilis Gorgoulis, Sébastien Lenglet, Fabrizio Montecucco, François Mach, Ulf Hedin, Göran K. Hansson, Claudia Monaco, Evangelos Andreakos
    Circulation, 2012
  • Treatment of viral conjunctivitis with antiviral drugs
    Chrysanthi L. Skevaki, Ioanna E. Galani, Michail V. Pararas, Konstantina P. Giannopoulou, Athanassios Tsakris
    Drugs, 2011
  • Antitumor vaccination by Newcastle Disease Virus Hemagglutinin-Neuraminidase plasmid DNA application: Changes in tumor microenvironment and activation of innate anti-tumor immunity
    Jing Ni, Ioanna E. Galani, Adelheid Cerwenka, Volker Schirrmacher, Philippe Fournier
    Vaccine, 2011
  • Regulatory T cells control macrophage accumulation and activation in lymphoma
    Ioanna E. Galani, Marco Wendel, Ana Stojanovic, Maria Jesiak, Margareta M. Müller, Carola Schellack, Elisabeth Suri-Payer, Adelheid Cerwenka
    International Journal of Cancer, 2010
  • Inhibition of constitutively activated nuclear factor-K,B induces reactive oxygen species- and iron-dependent cell death in cutaneous T-cell lymphoma
    Michael K. Kiessling, Claus D. Klemke, Marcin M. Kamiński, Ioanna E. Galani, Peter H. Krammer, Karsten Gülow
    Cancer Research, 2009
  • Mononuclear myeloid-derived "suppressor" cells express RAE-1 and activate natural killer cells
    Norman Nausch, Ioanna E. Galani, Eva Schlecker, Adelheid Cerwenka
    Blood, 2008
  • Natural killer cell accumulation in tumors is dependent on IFN-γ and CXCR3 ligands
    Marco Wendel, Ioanna E. Galani, Elisabeth Suri-Payer, Adelheid Cerwenka
    Cancer Research, 2008