A5057457997- COVID-19 Clinical Research Studies
- Immune cells in cancer
- Long-Term Effects of COVID-19
- Inflammasome and immune disorders
- Neuroinflammation and Neurodegeneration Mechanisms
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- SARS-CoV-2 and COVID-19 Research
- Phagocytosis and Immune Regulation
- Immune Cell Function and Interaction
- Inflammatory Biomarkers in Disease Prognosis
- Autoimmune and Inflammatory Disorders Research
- Immune Response and Inflammation
- Dermatological and COVID-19 studies
- Pancreatitis Pathology and Treatment
- Nanoplatforms for cancer theranostics
- Immune responses and vaccinations
- Mangiferin and Mango Extracts
- Autophagy in Disease and Therapy
University of Verona
2020-2023
The San Raffaele Telethon Institute for Gene Therapy
2023
Biomedical Research Foundation of the Academy of Athens
2018
BACKGROUND. Patients with coronavirus disease 2019 (COVID-19) develop pneumonia generally associated lymphopenia and a severe inflammatory response due to uncontrolled cytokine release. These mediators are transcriptionally regulated by the JAK/STAT signaling pathways, which can be disabled small molecules.
Pulmonary thrombosis is observed in severe acute respiratory syndrome coronavirus 2 pneumonia. Aim was to investigate whether subpopulations of platelets were programmed procoagulant and inflammatory activities disease 2019 (COVID-19) patients with pneumonia, without comorbidities predisposing thromboembolism. Approach Results: Overall, 37 28 healthy subjects studied. Platelet-leukocyte aggregates, platelet-derived microvesicles, the expression P-selectin, active fibrinogen receptor on...
Since the beginning of SARS-CoV-2 pandemic, COVID-19 appeared as a unique disease with unconventional tissue and systemic immune features. Here we show signature associated severity by integrating single-cell RNA-seq analysis from blood samples broncho-alveolar lavage fluids clinical, immunological functional ex vivo data. This is characterized lung accumulation naïve lymphoid cells expansion activation myeloid cells. Myeloid-driven suppression hallmark evolution, highlighting arginase-1...
Myeloid cells can restrain antitumor immunity by metabolic pathways, such as the degradation of l-arginine, whose concentrations are regulated arginase 1 (ARG1) enzyme. Results from preclinical studies indicate important role arginine metabolism in pancreatic ductal adenocarcinoma (PDAC) progression, suggesting a potential for clinical application; however, divergent evolution ARG1 expression and function rodents humans has restricted translation. To overcome this dichotomy, here, we show...
Myeloid-derived suppressor cells (MDSCs) densely accumulate into tumors and potently suppress antitumor immune responses, promoting tumor development. Targeting MDSCs in immunotherapy has been hampered by lack of understanding the molecular pathways that govern MDSC differentiation function. Herein, we identify autophagy as a crucial pathway for MDSC-mediated suppression immunity. Specifically, patients with melanoma mouse exhibited increased levels functional autophagy. Ablation myeloid...
Abstract Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of ongoing pandemic disease 2019 (COVID-19). The majority patients with COVID-19 have a good prognosis, but variable percentages in different countries develop pneumonia associated lymphocytopenia and severe inflammatory response due to uncontrolled release cytokines. These immune mediators are transcriptionally regulated by JAK-STAT molecular pathways, which can be disabled small molecules. Here, we...
Abstract Inflammatory responses rapidly detect pathogen invasion and mount a regulated reaction. However, dysregulated anti-pathogen immune can provoke life-threatening inflammatory pathologies collectively known as cytokine release syndrome (CRS), exemplified by key clinical phenotypes unearthed during the SARS-CoV-2 pandemic. The underlying pathophysiology of CRS remains elusive. We found that FLIP, protein controls caspase-8 death pathways, was highly expressed in myeloid cells COVID-19...
Abstract Since the beginning of SARS-CoV-2 pandemic, COVID-19 has appeared as a unique disease with unconventional tissue and systemic immune features. While severe forms share clinical laboratory aspects various pathologies such hemophagocytic lymphohistiocytosis, sepsis or cytokine release syndrome, their exact nature remains unknown. This is severely impeding ability to treat patients facing stages disease. To this aim, we performed an in-depth, single-cell RNA-seq analysis more than...
Abstract Inflammatory responses rapidly detect pathogen invasion and mount a regulated reaction. However, dysregulated anti-pathogen immune can provoke life-threatening inflammatory pathologies collectively known as cytokine release syndrome (CRS), exemplified by key clinical phenotypes unearthed during the SARS-Cov-2 pandemic. The underlying pathophysiology of CRS remains elusive. We found that FLIP, protein controls caspase-8 death pathways, was highly expressed in myeloid cells COVID-19...