Speaker' information

Dr. John E. Eriksson is a Professor of Cell Biology and Director of Euro-BioImaging ERIC (www.eurobioimaging.eu), the pan-European organization of advanced biological and biomedical imaging, with Headquarters in Turku, Finland. Beyond making Euro-BioImaging the leading gateway to European imaging excellence, one of his pronounced ambitions, is also to generate a continuum from advanced imaging of diseases states with big data from omics and biobanks using the vast imaging resources of Euro-BioImaging and active collaboration with other major European and global life science research infrastructure and data-related organizations. By combining advanced imaging technologies with other cutting-edge molecular technologies, his research team has unraveled a selection of cellular signaling networks that determine critical cell responses for human health, including activation of survival mechanisms, cell growth, differentiation, and cell migration. Some of the findings have also led to innovations in both drug development and biomaterial sciences that have resulted in a number of international patents including a recent start-up company. He has published more than 200 scientific articles, numerous patents, and is an elected member of the Finnish Society of Sciences and the Technical Science Academy of Finland.

BS, 1995, First National Prize; PhD and First Class Honours distinction, 2003. I performed my clinical specialization in Immunology (1996-2000) and my PhD (2000-2003) in La Princesa Hospital/UAM. I took a postdoctoral position at the London Research Institute (Cancer Research UK, 2004-2009) where I found a new C-type lectin (DNGR-1/CLEC9A) that marks the population of human and mouse dendritic cells (DCs) that cross-present antigens in MHC-I, using this selective expression to target DCs for tumor immunotherapy (JCI, 2008). Our work additionally established the function of DNGR-1/CLEC9A in cross-priming in vivo (Nature, 2009).My current research centres on myeloid cells, the molecular mechanisms they utilise to detect infection, tissue damage and cancer and how this impacts immunity to infection, inflammatory/autoimmune diseases and cancer. We identified DNGR-1 (CLEC9A) as a receptor highly restricted to conventional type 1 dendritic cells (cDC1s) that could be targeted for anti-tumor therapy (JCI 2008). DNGR-1 binds to dead cells and allows cDC1 retrieve antigens from cell corpses for cross-presentation (Nature 2009). This facilitates CD8+ T cell responses to cytopathic viruses (JCI 2012) and contributes to priming of precursors of resident memory CD8+ T cells (Trm) (Immunity, 2016b), key cells that contribute to anti-tumor immunity (Nat. Commun. 2017). Notably, we found that C-type lectin receptors with activating motifs can also bind tyrosine phosphatases and inhibit immunity and inflammation (Science 2018; Cell Reports 2018; Immunity, 2016a) and regulate host-microbiota interactions (Immunity 2019). In related work, we advanced our understanding of the relevance of cDC1s in pathologies like Leishmania infection (Eur. J. Immunol. 2015), asthma (JCI insight 2017), cancer (Cancer Discov. 2016; JITC 2019; JITC 2021) and obesity (Cell Mol Immunol 2022).Our current research focuses on the crosstalk of mitochondrial metabolism and function of myeloid cells. We have shown that innate immune sensing by macrophages can repurpose mitochondrial metabolism and modulate macrophage function and polarization (Nat. Immunol. 2016; Nat. Metab. 2020). Further, macrophage function in tissues is tightly regulated by mitochondrial respiration depending on the organ microenvironment (Immunity 2023). We are also exploring the molecular pathways controlling trained immunity in macrophages (Cell Reports 2018a; Cell Reports 2018b; Front. Immunol 2021; Cell Reports 2022) and its connection to atherosclerosis. Additionally, we are investigating the role of gut microbiota and its metabolites in the progression of atherosclerosis and exploring their diagnostic, mechanistic, and therapeutic potential.

This research has been funded by an ERC Starting Grant (2010), ERC Consolidator Grant (2016), a Horizon 2020 consortium on cancer immunotherapy, collaboration with companies, including Medimmune, Inmunotek, LeadArtis and Adendra Therapeutics and also public and private national funding, including a Caixa Foundation Grant.

Indicators of quality in Scientific productionPublication number (WOS): 130 (49 as main author, MA); first quartile (Q1): 106 (38 MA), first decile (D1): 72 (29 MA); top 3: 31 (11 MA). Citations: >11,500 (>91 citations per item, WOS & Scopus); >16,000 (G. Scholar); H index: 56 (WOS & Scopus); 64 (G. Scholar). Over 1500 citations per year in the last two years.

She graduated with a Master’s degree in Biochemistry and Microbiology from Sofia University, where her research at the Institute of General and Comparative Pathology under Rajna Tosheva’s mentorship laid the groundwork for her future career. She then pursued her PhD in Biochemistry and Biophysics at Washington State University, mentored by Norman G. Lewis and Laurence B. Davin, further solidifying her expertise in the molecular underpinnings of life.

Her journey continued with postdoctoral training in Pharmacology and Molecular Sciences at Johns Hopkins University School of Medicine, working alongside the renowned Paul Talalay. This experience deepened her understanding of how drugs and natural compounds interact with biological systems, setting the stage for her groundbreaking research in disease prevention.

In 2007, Dinkova-Kostova joined the University of Dundee as a Research Councils UK Academic Fellow and research group leader. Her lab, at the interface of chemical biology and medicine, has become a hub of innovation, collaborating with scientists, clinicians, and the pharmaceutical industry to decipher the complex interplay between cells and their environment.

A major focus of her research is the Keap1/Nrf2 pathway, a critical cellular defense mechanism that protects against oxidative and inflammatory damage. By unraveling the intricate regulation of this pathway and identifying compounds that can modulate its activity, Dinkova-Kostova’s team is paving the way for new preventive and therapeutic approaches for cancer and other chronic diseases.

Her investigations extend beyond the Keap1/Nrf2 pathway to explore the heat shock response, another key cellular defense mechanism, and the potential of inhibiting heat shock protein 90 (Hsp90) to disrupt cancer cell growth. Her team employs a multi-faceted approach, utilizing biochemical techniques, cellular models, and in vivo studies to gain a comprehensive understanding of these processes.

Recognition and Impact

Dinkova-Kostova’s contributions to science have garnered numerous accolades. She is the recipient of the prestigious 2011 Arthur C. Neish Young Investigator Award from the Phytochemical Society of North America and has been recognized as a Highly Cited Researcher by Clarivate for several consecutive years. In 2023, she was elected a Fellow of the Royal Society of Edinburgh, followed by her election as a Fellow of the Royal Society of Biology in 2024, underscoring her significant impact on the scientific community.

Her research has not only advanced our fundamental understanding of cellular defense mechanisms but has also translated into tangible benefits for patients. Two pharmacological Nrf2 activators, inspired by her work, have entered clinical practice for the treatment of multiple sclerosis and Friedreich’s Ataxia, highlighting the real-world impact of her discoveries.

Ioannis Trougakos obtained his Ph.D. in Cellular-Developmental Biology from the National and Kapodistrian University of Athens (NKUA), Greece. He has worked as Research Scientist at EMBL, Germany, CBM “Severo Ochoa”, Spain and at NHRF, Athens, Greece; he was also research visitor at EMBL and at the Netherlands Cancer Institute. Dr. Trougakos was elected Research Lecturer at NHRF and currently he serves as Professor and Director of the “Cell Biology” lab at the Faculty of Biology, NKUA. He is the Head of the “Ageing and Age-Related Diseases” group (http://scholar.uoa.gr/itrougakos). Dr. Trougakos has published articles in high-ranking journals, chapters in international books; he is also co-inventor in several patents. His group is funded by private (GR, EU, USA) and public (GR, EU) entities; also, the group participates in contractual activities with the Industry.

The study of genetics, B-cell receptor (BCR) repertoire, and signaling has led to significant advancements in understanding mature leukemias and lymphomas, such as chronic lymphocytic leukemia (CLL). Leukemias and lymphomas are characterized by complex genetic backgrounds. Having said that, key mutations and genetic alterations have been identified, including those in NOTCH1, SF3B1, and TP53 genes. Furthermore, continuous efforts did lead to the characterization of additional relevant variants, including those in the RPS15 and NFKBIE genes, which are linked to disease progression and resistance to therapy. Recent immunogenetic research has demonstrated that the BCR repertoire in CLL exhibits restricted diversity and stereotypy, indicating that specific antigens may drive the disease\\\’s development and progression. This BcR-based stereotypy correlates with particular genetic abnormalities and clinical outcomes, providing valuable prognostic information for CLL patients. Investigations into BCR signaling have shown that it is crucial for the survival and proliferation of CLL cells. In more specific, aberrant BCR signaling contributes to the pathogenesis of CLL and represents a potential therapeutic target. Overall, these findings have enhanced the understanding of the interplay between leukemia genetics, BCR repertoire, and BCR signaling, with significant implications for the diagnosis, prognosis, and treatment of CLL. This research paves the way for more effective and tailored therapeutic approaches, ultimately improving patient outcomes. Finally, these areas od research have proved instrumental in understanding the ontogenesis of leukemia, especially in the context of monoclonal B cell lymphocytosis (MBL). MBL is considered a pre-leukemic condition that is very common in the general population. Comparative analysis between CLL and MBL at the genetic, immunogenetic and cell functional levels have assisted in the identification of those molecular and cellular mechanisms that contribure significantly in the onset of leukemia.