Victor Appay is Research Director at the National Institute of Health and Medical Research (INSERM - France) and Professor at Kumamoto University (Japan). He obtained his Ph.D in Immunology at the Institute of Molecular Medecine (Oxford, UK) in 2001. He is heading the research team “HIV Pathogenesis and Immune Aging” at the Centre d’Immunologie et des Maladies Infectieuses (CIMI-Paris) at Sorbonne University. Over the last 20 years, his work has been primarily focused on the study of T-cell immunity. He has made seminal observations on the efficacy of T-cell immunity against viruses and tumors, and its decline in the context of chronic viral infections or aging. A central topic of his research is on better understanding the exhaustion of immune competence with human aging. His team aims at characterizing further the hematopoietic resources in the elderly and explore the potential causes of their decline in relation to elevated inflammation, and at studying the consequences of this primary immune resource exhaustion on adaptive and innate immunity in humans.
Centro de Investigaciones Biológicas, CIB-CSIC, Madrid
Patricia Boya studied biology at the University of Texas at Austin (USA), and Universidad de Navarra, where she got a PhD degree on cell biology in 2000. Postdoc as a Marie Curie fellow t at the laboratory of Guido Kroemer in Paris, setting set up all the tools for autophagy research and discovering the cytoprotective role of autophagy in mammalian cells. Patricia returned to Spain in 2005 with a Ramón y Cajal contract at the CIB in the Spanish Research Council (CSIC). She obtained a permanent position at CSIC in 2008 and have promoted to Assistant Professor in 2016. She is the first President of the Spanish Autophagy Society SEFAGIA that has gathered the autophagy community in Spain since 2013. She is also core group member of the COST Action Transautophagy and the ITN DRIVE focused on Autophagy.
Her lab uses cellular and animal models to understand the physiological roles of autophagy and its implications during disease in the nervous system using the retina as a model. Currently, their main focus is to understand how the selective elimination of mitochondria by autophagy (also known as mitophagy) impacts cell homeostasis. In particular, they are interested in how mitophagy may influence mitochondrial health and the consequences for cell survival and death and tissue homeostasis in the nervous system in both physiological and pathological conditions.
Graduated in Biomedicine and Master's on Neuroscience by Federal Fluminense University (Brazil). phD in Biophysics by Federal University of Rio de Janeiro (Brazil). Postdoctorate in University of Chile in collaboration with the Buck Institute for Research on Aging (USA). Expertise on molecular neuroscience and cellular biology with emphasis on neuronal plasticity, neuronal death, cellular stress, endoplasmic reticulum stress and proteostasis. Dedicated the last years to understand the aging process of the brain aiming to slow down the cognitive and motor decline associated to the normal process of aging and its transition to pathological states such as Alzheimer's disease and other neurodegenerative diseases
Flavie Coquel is an engineer from the Université de Technologie de Compiègne. She got her Ph.D. at the Institute of Human Genetics (Université de Montpellier), under the supervision of Dr Philippe Pasero and Dr Yea-Lih Lin. In the laboratory of Dr Philippe Pasero, she studied the response to DNA replication stress. She contributed to better understand how mutations in the protein SAMHD1 cause the Aicardi Goutières Syndrome, a rare inflammatory disorder. She also worked on the modulation of DNA replication stress in order to target cancer cells. She obtained a 2018 Young Researcher prize from the Jérôme Lejeune foundation and a 2018 L’Oréal-UNESCO prize for Women in Science for this work.
She is now a post-doctorate fellow in the laboratory of Prof. Andrea Ablasser (Ecole Polytechnique Fédérale de Lausanne) where she investigates the interplay between genome maintenance mechanisms and the innate immune response.
Trained first as a biologist, then as endocrinologist and as an immunologist, David Dombrowicz, PhD, is Research Director from Inserm (French National Institute of Health) and Team Leader in Unit 1011 (Inserm, Institut Pasteur de Lille, University of Lille and University Hospital of Lille) “Nuclear Receptors, Metabolic and Cardiovascular Diseases”. In the field of immunology, D. Dombrowicz and his group made seminal contributions in the understanding of the cellular and molecular mechanism of allergic diseases and immunoregulation. Early studies were focused the role of the high affinity IgE receptors and low affinity IgG receptors in anaphylactic reactions and intestinal inflammation. Research then investigated the contribution of polynuclear eosinophils in allergic asthma and atopic dermatitis, both in humans and in animal models, and the immunoregulation of these pathologies as well as anaphylaxis in particular through prostaglandin receptors, nuclear receptors (PPAR) and chemokine receptors. Moving to immunometabolism, research interests focussed on the regulation of immune function by "metabolic" nuclear receptors (the bile acid receptors, FXR, and RORα) and its impact on metabolic diseases. Most recent work has investigated the basic mechanisms underlying comorbidities between asthma or psoriasis and metabolic diseases with a particular interest on the role of fatty acids as modulators of immune response and the contribution of immune cells to NonAlcoholic SteatoHepatitis (NASH). D. Dombrowicz work has been published in leading journals such Cell, Nat. Med., Immunity, Nat. Met., Nat. Rev. Immunol….
I am a trained molecular biologist and microbiologist, with expertise in immunology, cancer research and a strong link to translational research evoked by 10 years of work and expertise in a Pathology Institution (Clinical Pathology, University Hospital Zurich, Switzerland).
Since 2015 I am a W3 Professor at the University Heidelberg and Department Head at the German Cancer Research Center (DKFZ) in Heidelberg, Germany, focusing on the link between chronic inflammation and cancer, with the main focus on inflammation driven liver cancer (see also https://www.dkfz.de/de/chronische-entzuendung-und-krebs/index.php).
Our laboratory aims at understanding the different immune signatures of chronic inflammatory human diseases (e.g. induced through dietary or viral etiologies) driving tissue damage, autoimmunity and cancer using patient material and relevant pre-clinical mouse models for functional studies. Moreover, we try to understand the systemic functional effects of pathologies and the interplay between several affected non-lymphoid tissues, the gastrointestinal tract and the immune system (e.g. liver-gut axis; muscle-liver axis; liver-brain axis). We focus on comparative studies of tissue specimen of human patients and animal models, recapitulating human disease on a histopathological and pathophysiological level. Our main focus is the understanding of the pathophysiology of primary and metastatic liver cancer and possible treatment thereof. We engage in classical molecular biology techniques complemented with sophisticated ways to receive as much information as possible from tissue samples through histology (e.g. light microscopy/ immune fluorescence/ FISH/RNA in situ hybridization), histo-cytometry (a combination of Flow cytometry and histology), single cell analysis and other in vivo imaging techniques (e.g. MRI, IVIS, ultrasound) as well as through FACS analyses of tissue homogenates. At the same time we perform single cell analyses in situ and have established a novel technology to analyze the metabolome on single cell level (single cell metabolomics in situ). Finally, we engage in long-term 3D cultivation techniques of primary patient and mouse tissue (e.g. liver) in order to perform infection studies (e.g. HBV/HEV/HAV) as well as genetic/ interventional studies.
We test several therapeutic compounds in single but also combinatorial fashion (e.g. novel immune check point inhibitors) employing newly established or stratified pre-clinical mouse models. Moreover, we engage in clinical trials and currently generate our first GMP-produced nanobody - with the aim to bring this treatment into the clinic (e.g. Malehmir et al., Nature Medicine 2019). Recently, our research was rated the third most cited in German speaking countries in the field of “Cell Biology” from 2012 - 2016.
Dr JP Hugot is Professor of pediatrics at the Faculty of Medicine Paris Diderot-Sorbonne and head of the department of paediatric gastroenterology and nutrition at Hôpital Robert Debré, APHP, Paris. He is also director of the INSERM Research team “gut inflammation”, UMR1149, Faculté Bichat, Paris. He discovered the first and main Crohn Disease susceptibility gene (NOD2). This gene was the first example of the identification of a susceptibility gene by a positional cloning strategy in complex genetic disorders. This paper has received more than 3000 citations. It was followed by many contributions on the genetics of inflammatory bowel diseases including GWAS, genotype/phenotype correlation studies; disease risk, etc. He demonstrated the role of NOD2 on the intestinal barrier providing a comprehensive model on how Nod2 contributes to the development of Crohn Disease in mutated people. More recently, he developed a comprehensive theory on gene-environment interactions in Crohn Disease based on the idea that industrialised and/or refrigerated food could explain the outbreak of Crohn Disease in developed countries.
Frank Lafont has been trained as a neurobiologist at the École Normale Supérieure (Paris, France) during his PhD obtained at the Univ. Pierre et Marie Curie. Then, he learned Cell Biology at European Molecular Biology Laboratory (Heidelberg, Germany) working on the membrane trafficking of viral proteins. He started his cellular microbiology research project based on bacteria interaction with the host cell focusing on raft membranes at the University of Geneva, Univ. Medical Center (Switzerland) and learned Atomic Force Microscopy at the École Polytechnique Fédérale de Lausanne (Switzerland) to study the physics of these membrane domains.
Since 2005, he is group leader at the Pasteur Institute in Lille where he developed a multidisciplinary approach to study how pathogens hijacked autophagy during infection, and how they interact with the host cell with an emphasis more at the membrane interfaces. In particular, the Cellular Microbiology and Physics of Infection group unveiled how membrane damages are regulated by LC3-dependent mechanisms and how pathogenic bacteria subvert the autophagy pathway to their own benefit. To address these biological questions, the group has pioneered and developed several methodological methods such as membrane stiffness tomography and correlative methods based on Atomic Force Microscopy.
Frank Lafont has also a degree from the École Supérieure de Commerce de Paris-Europe with major in management and is heading the BioImaging Center Lille high technology Facility. He is coordinating and member of many national and international programs and is strongly involved in teaching Biology and in Physics at the Univ. Lille notably. He is deeply implicated in technological networks and science popularization. Frank Lafont has been member of many authorities, including at the CNRS Life Science National Institute in charge of the host-pathogen interactions field.
Dr. Oury is a graduate of Louis Pasteur University in Strasbourg (France), where he trained in the field of neurobiology in the laboratory of Dr. Filippo Rijli (Institut de Génétique et Biologie Moléculaire et Cellulaire (IGBMC)). His doctoral work demonstrated the crucial role of the homeobox transcription factors for the establishment of the sensory neuronal connectivity. He then moved to Columbia University, New York, USA, in the laboratory of Gerard Karsenty, where he gained expertise in neuro- and integrative-physiology, identifying novel endocrine functions of the skeleton in regulating gonadal, pancreatic and brain functions. Since 2014, he joined the Institute Necker (INEM) as a group leader. The main research interest of his team is to understand and characterize how brain functions are modulated by hormonal factors in normal, pathological and aging conditions. He recently focused on the role of neuronal autophagy has an essential intracellular mediator mechanism of the effect of systemic factors and its impact on brain cognitive fitness, plasticity and aging processes.
Dr. Oury is a laureate of the Foundation Schlumberger (FSER) award, the Blavatnick award (USA), the Rupert Timpl Award (Netherlands), the Longevity award Allianz-ADPS and the ATIP-AVENIR program.
After a PhD work in the George Thomas laboratory (Friedrich Miescher Institute, Basel, Switzerland), Mario Pende moved to Paris Descartes University and was awarded the INSERM AVENIR contract in 2002, and became tenured PI in 2007. He received the ERC-starting and consolidator grants in 2008 and 2013, respectively.
Mario Pende has been interested in how nutritional cues are transduced in the cell to impact growth and ageing responses, including cell size, cell proliferation, senescence, protein synthesis and metabolism. His main achievements in this field are the following:
1) identification of S6K1 and S6K2, and discovery of a cell size defect in loss-of-function mutants (Pende et al., Nature, 2000; Ohanna et al., Nature Cell Biol., 2005)
2) impact of mTOR/S6K activities on metabolic adaptations and senescence (Aguilar et al, Cell Metabolism 2007; Barilari et al., EMBO J., 2017)
3) involvement of this pathway in tumour development (Panasyuk et al., Nature Comm., 2012; Liang et al., J Exp Med, 2014)
Born April 30, 1944 in Split (Croatia). Citizen of Croatia and France; resident of France.
Currently professor emeritus of cell biology at the Medical School of the Rene Descartes University – Paris-5. Co-founder and research director of the Mediterranean Institute of Life Sciences (MedILS (www.medils.hr) in Split, Croatia. former science adviser to the Prime Minister of Croatia. Member of the French « Academie des Sciences », American Academy of Arts and Sciences, Croatian Academy of Sciences and Arts, Academia Europaea, World Academy of Arts and Sciences, the European Molecular Biology Organization (EMBO) and the National Academy of Sciences (NAS).
Recipient of over a dozen of major international and national science awards. Keynote or plenary speaker at 48 international congresses, invited speaker to over 300 international science meetings. Gave over 600 lectures and seminars worldwide. Knighted by the Presidents of France and Croatia.
Published over 200 research and review articles in the areas of DNA repair, DNA replication, mutagenesis, genetic recombination, evolution, microbiology and cancer research, that were cited over 10.000 times. Three discoveries (SOS system, mismatch repair and molecular basis of the genetic barriers between related species) are present in the basic genetics and molecular biology textbooks. Up to 200.000 Google entries.(more at: www.miroslavradman.com).
Dr Léa Rémy-Tourneur is Associate Professor of Cellular Biology and Immunology at the Paris Descartes University. Since September 2019, she performs her research activity at the Cochin Institute in the team of Dr Véronique Witko-Sarsat.
Léa Tourneur studied in Immunology at the Cochin Institute at Paris in the team of Dr Gilles Chiocchia. Rapidly, she focused her research on the Fas-associated death domain (FADD) protein that is the key adaptor molecule for the death receptors of the tumor necrosis factor receptor superfamily. She defended her PhD thesis in 2002 at the Paris Descartes University, and continued to study the mechanisms contributing to the FADD protein expression regulation during her postdoctoral fellowships. At the end of 2007, she was recruited at the Paris Descartes University as an associate professor. She graduated her HDR in 2014.
During the past years, she confirmed that FADD protein could act as a tumor suppressor. She showed that FADD protein expression could be lost in mouse and human cancer cells and could be used as a prognostic factor for poor response to chemotherapy. Moreover, she identified for the first time that FADD protein can be secreted in the extracellular space. The release of FADD by human lung cancer cells could be a new marker of poor prognosis as it correlates positively with both tumor progression and aggressiveness. More recently, she demonstrated that monocytes/macrophages unconventionally secreted the FADD protein in response to the NLRP3 inflammasome activation, and established human secreted FADD as a new marker of joint inflammation in gout and rheumatoid arthritis, two rheumatic diseases. Thus, she identified the FADD protein and FADD protein secretion as potential therapeutic targets at the crossroads between cancer and inflammation.
Senescence as a therapeutic target for myocardial ageing and disease.
Gavin Richardson is a Research Fellow and group leader in the Cardiovascular Research Centre in the Institute of Genetic Medicine at Newcastle University, UK. Following the award of a PhD in Stem Cell Biology in 2004, Gavin studied skin dermal stem cells and skin ageing at Durham University, with sabbaticals at Columbia and Harvard Universities. In 2011 Gavin moved back to Newcastle University as an Independent Research Fellow, and applied his expertise in regeneration and ageing to the heart. His research aims to understand how senescence and attenuated regeneration contribute to the pathophysiology of maladaptive myocardial remodelling that occurs during ageing or as a result of myocardial infarction. His aim is to identify novel therapeutics targeting these processes to improve cardiac function in patients.
Bernard Thorens is Professor at the Center for Integrative Genomics of the University of Lausanne. He graduated in biochemistry from the university of Geneva where he also obtained a Ph.D in molecular immunology. He did a five-year postdoctoral fellowship at the Whitehead Institute for Biomedical Research, Cambridge, USA, before joining the University of Lausanne as an assistant professor. He is recognized for his work on the molecular physiology of glucose transporters and of gluco-incretin receptors, which he initiated by the cloning and functional characterization of the beta-cell glucose transporter Glut2, and of the pancreatic beta-cell GLP-1 receptor. He is now focusing on the study of neuronal glucose sensing in the control of glucose homeostasis and feeding behavior. He also investigates novel intracellular signaling pathways that control pancreatic beta-cell mass and function, in particular in response to gluco-incretin hormones and metabolic stress.
His work has been continuously funded by Swiss and European grants, including Advanced Research Grants from the European Research Council. He is coordinator of EU Innovative Medicine Initiative grants (RHAPOSDY, and previously of IMIDIA). He served as vice-president of the EASD (2012-2015). He is an elected member of the Research Council of the Swiss National Science Foundation and of the Swiss Academy of Medical Sciences. His work has been recognized with several national and international awards, including the 2009 Albert Renold Award from the EASD for his work on pancreatic beta-cells and the 2017 Claude Bernard Award from the EASD for his lifetime achievements in the field of diabetes research.
EVP and Head of Research, Genfit SA
Robert WALCZAK (Ph.D.) is a senior director and head of research at Genfit SA, a biopharmaceutical company that develops pioneering therapeutic and diagnostic solutions in chronic liver diseases. For the last 15 years, his activity was focused on drug discovery and drug repurposing programs in the fields of NASH and hepatic fibrosis. His research objective is to provide drug candidates with optimized bench to bedside translatability potential by using highly innovative phenotypic screening approaches in primary cells and in reconstituted liver microtissues.
Dr. WALCZAK graduated from Pasteur University in Strasbourg (FR) and accomplished his post-doctoral training at the University of Lausanne (CH) and then at Howard Hughes Medical Institute (USA), where he worked on a role of nuclear receptors as drug targets in metabolic diseases.