Andrea Ablasser, École Polytechnique Fédérale De Lausanne (EPFL), Switzerland

Dr. Ablasser heads a lab at the EPFL in Lausanne, Switzerland.

The Ablasser Lab aims to understand how the cells of our immune system detect pathogens, and to dissect the fundamental mechanisms that provide host defense. Recently, Dr. Ablasser’s group has made some vital discoveries in the cGAS-STING cytosolic DNA sensing pathway.

Geir Bjørkøy, CEMIR, NTNU, Norway

Geir Bjørkøy is a professor at the Department of Biomedical Laboratory Science at the Norwegian University of Science and Technology (NTNU) in Trondheim.

Bjørkøy was central for defining the first autophagy cargo receptors that enable selective degradation of intracellular components. These studies also provided novel markers for how to measure autophagic flux. The Bjørkøy group now focus on how autophagy is regulated in cancer and stroma cells during formation of solid tumours.  In particular, the group study how nutrient restriction within solid tumours may result in cell specific changes in autophagy and how such changes might support survival and growth of the cancer cells. The studies includes how cancer cells secrete signaling substances to induce protein catabolism and mobilize nutrients from stroma cells. Of special interest is if this may be relevant for muscle wasting in cancer patients. Also, the group investigate how autophagy in cancer and innate immune cells may shape the local immune environment within solid tumours.

Aline Bozec, Friedrich-Alexander-University Erlangen-Nürnberg, Germany

Aline Bozec is a professor at Friedrich-Alexander-University Erlangen-Nürnberg (FAU) at the Department of Internal Medicine 3, Rheumatology and Immunology at Universitätsklinikum Erlangen.

She studies the crosstalk between metabolism, bone homeostasis and inflammation. A research goal is to identify new target genes which could link obesity and diabetes to osteoporosis on one side and to inflammatory diseases such as rheumatoid arthritis on the other side.

Petr Broz, Department of Biochemistry, University of Lausanne, Switzerland

Petr Broz is an Associate Professor at the Department of Biochemistry, University of Basel, Switzerland.

He has been working on bacterial type 3 secretion systems with Guy R. Cornelis before he joined the laboratory of Denise Monack in 2008, where he started to work on inflammasome complexes in the context of bacterial infections. In 2013 he returned to Basel where he currently investigates inflammasome activation and the induction of pyroptosis, a lytic, inflammatory cell death.

Ken Cadwell, NYU School of Medicine, USA

Cadwell is a Principal Investigator at the New York University School of Medicine.

The Cadwell Lab focus on how the normal balanced co-existence between intestinal microbes and the host immune system is disrupted during disease. In particular, the group study how common gene variants contributes to increased diseases susceptibility because their role becomes apparent only in the presence of certain environmental factors. The ATG16L1 gene encodes a protein crucial for autophagy and a variant of this gene is a risk factor for developing infections bowels disease (IBD).

The group have described how host responses to murine norovirus depends on the genotype of the ATG16L1 gene and now study how Atg16L1 determines the quality and magnitude of the immune response to intestinal viruses and bacteria. The investigations includes the relationship between autophagy and inflammation and the function of other IBD susceptibility genes such as Nod2 in disease development.

Trude Helen Flo, CEMIR, NTNU, Norway

Professor and Co-Director of Centre of Molecular Inflammation Research (CEMIR) at NTNU.

The primary research focus is the molecular host defense mechanisms involved in immunity to mycobacteria and HIV and virulence strategies employed by the pathogens to parasitize host cells. Intracellular trafficking, compartmentalized pattern recognition receptor signaling, host cell killing and nutrient metabolism are central for survival and attractive targets for drug development, and are currently investigated in the host and in the pathogen.

Douglas Golenbock, UMass Medical School, USA

Professor at University of Massachusetts Medical School and Chief of the Division of Infectious Diseases and Immunology.

The goal of his laboratory is to characterize phagocytic receptors that recognize the presence of microbes in the context of infectious illnesses. As the mechanisms of inflammation in infectious diseases are similar to those associated with sterile inflammation, the group also studies Alzheimer's Disease. Their work focuses on two groups of receptors: Toll-like receptors (TLRs) and Nod-like receptors (NLRs) in the context of the inflammasome.

Warner C. Greene, Gladstone institutes, USA

Warner C. Greene, MD, PhD is Director and Professor of Translational Medicine at Gladstone Institute of Virology and Immunology, and Professor of Medicine, Microbiology and of Immunology at UCSF.

Dr. Greene’s work seeks to understand the interplay of human retroviruses like HIV and HTLV with their cellular hosts, to find new approaches for prophylaxis and therapy. Dr Greene and coworkers have shown that most CD4 T cells die due to an innate immune response against cytoplasmic viral DNA accumulating after abortive HIV infection. Other studies focus on mechanisms underlying HIV latency including a role for host proteins and miRNAs, as well as proteins such as NF-kB that antagonize latency.

Veit Hornung, Gene center Munich, Germany

Veit Hornung is Professor of Immunology at Gene Center, Ludwig-Maximilians-Universität München.

In his work, Dr-Hornung tries to decipher relevant MAMP or DAMP molecules during infection or sterile inflammation, identify novel PRRs, signalling cascades and their functional roles. He has studied how nucleic acids are sensed by PRRs, and effector functions. This includes compartmental strategies for some microbe-derived nucleic acids such as e.g. detection of double stranded DNA by the cGAS-STING axis in the cytosol. Since nucleic acid detection is tightly connected to the type I IFN system, insight into nucleic acid sensing PRR systems opens new avenues for the development of therapies that activate the immune system.

Claudia Kemper, The National Heart, Lung, and Blood Institute (NHLBI), USA

Kemper is a Professor at King's College London. The Kemper Lab studies the role of complement in immunological and inflammatory processes, how the complement system instructs and guides the adaptive immune response is a major research interest.

The description of complement-induced regulatory T cells provided a novel link between the complement system and T cell responses. The ultimate goal is the design strategic clinical therapies that regulate the activity of Th1 cells based on local, T cell derived complement activation fragments.

Eicke Latz, Institute of Innate Immunity, Germany

Director of Institute of Innate Immunity, Bonn.

Latz is a leader in the field on innate immunity and inflammasome biology. His research focusses on identifying the mechanisms of innate immune activation in chronic inflammatory diseases and the influence of diet on inflammation. In addition, his lab also works on understanding the anti-inflammatory TAM receptors signaling pathway.

Egil Lien, University of Massachusetts (UMass), USA

Dr. Egil Lien earned his PhD from NTNU in 1998 and is currently Professor at University of Massachusetts, USA.

The laboratory of Egil Lien studies innate immune responses mainly to bacterial pathogens. A key focus is evasion mechanisms bacteria can employ to manipulate innate immune responses, and counter-measures from the host. Central model systems are Yersinia and Salmonella bacteria, and the goal is to better understand how they interact with innate signaling components such as inflammasomes, caspases, gasdermins and TLRs.

Katrin Mayer-Barber, NIH, USA

Dr. Katrin D. Mayer-Barber is a group leader and chief of the Inflammation and Innate Immunity Unit at the Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases.

She studies the function and regulation of inflammatory cytokines and lipid mediators during pulmonary infections, the immunological mechanisms of host protective versus host detrimental inflammation, and the translation of basic observations into host-directed immunotherapies.

Edward A. Miao, University of North Carolina School of Medicine, USA

Edward A. Miao, MD, PhD is associate professor at the University of North Carolina School of Medicine, Chapel Hill.

Miao has contributed seminal studies of how the innate immune system differentiates between pathogenic and non-pathogenic bacteria, and how programmed cell death is used as a defense against intracellular infection. His group studies a variety of bacterial pathogens that cause infection in the intestines, liver, as well as systemic infection (including Salmonella, Listeria, Burkholderia, and Chromobacterium).

Tom Eirik Mollnes, Univeristy of Tromsø, Norway

Tom Erik Mollnes is professor at the University of Oslo and at UiT The Arctic University of Norway.

The Mollnes Lab do research on the role of complement in human disease. A primary research goal is to elucidate the role of complement as a primary inducer of the inflammatory reaction. His work has focus on inflammatory diseases with emphasize on infection, sepsis and inflammatory response syndrome and ischemia-reperfusion injury.

Menno Oudhoff, CEMIR, NTNU, Norway

Dr. Oudhoff is one of the group leaders at CEMIR, the organizing research centre, in Trondheim, Norway.

The Oudhoff Lab aims to combine the fields of (intestinal) stem cell biology and regeneration with that of infection and immunity. Using in vivo and in vitro  models of intestinal disease the group studies cellular and molecular mechanisms of development and disease. 

Fiona Powrie, Kennedy Institute of Rheumatology (NDORMS), University of Oxford, United Kingdom

Dr. Powrie is a Professor in Musculoskeletal Sciences and is the Director of the Kennedy Institute in Oxford, UK.

Work in the Powrie lab is focused on understanding the interaction between the intestinal microbiota and the host immune system and how this mutualistic relationship breaks down in inflammatory bowel disease and cancer. Dr. Powrie’s work has been instrumental in identifying T cell subtypes, and is continuously making key discoveries in Mucosal Immunology.

Photo: Thomas S.G. Farnetti/Wellcome

Clare Pridans, University of Edinburgh, Scotland

Dr Clare Pridans is a principal investigator at the Centre for Inflammation Research at Edinburgh Medical School, Clinical Sciences.

Her research focuses on understanding the role of CSF1R signalling during macrophage development and also during postnatal development of the rat. To achieve this, she make use of rats deficient in CSF1 and CSF1R as well as CSF1R-mApple reporter transgenic rats. Initial studies have highlighted important differences between mouse and rat models and suggest that rat macrophages are more similar to humans than mice.

Felix Randow, MRC Laboratory of Molecular Biology, United Kingdom

Felix Randow is a Principal Investigator at University of Cambridge.

Cell autonomous innate immunity, i.e. the ability of individual cells to defend themselves against infection, is the major research interest in the Randow Lab. Projects in the laboratory focus on the role of the ubiquitin system and autophagy in the cytosolic defense against bacterial infection, the regulation of NFkB and IRF signaling and somatic cell genetics.

Anne Simonsen, University of Oslo, Norway

Anne Simonsen is Professor in Cell Biology at UiO where she is heading a research group on Autophagy. The focus is on identifying proteins required for targeting autophagic cargo for degradation using high-throughput siRNA screens, in combination with molecular, biochemical and cell biological assays, as well as model organisms. Simonsen is also co-directing the Centre of Excellence for Cancer Cell Reprogramming together with Harald Stenmark.

Therese Standal, CEMIR, NTNU, Norway

Therese Standal is a professor at the Department of Clinical and Molecular Medicine at the Norwegian University of Science and Technology (NTNU) in Trondheim.

She studies how cancer and inflammation influence bone homeostasis. The major goal is to understand why multiple myeloma patients loose bone.

Harald Stenmark, Oslo Univeristy hosptial, Norway

Professor and director of the Centre for Cancer Cell Reprogramming, University of Oslo.

Stenmark is an expert in the field of intracellular sorting and trafficking mechanism. His research focus is on basic cell biological mechanisms of endocytosis, autophagy, cytokinesis and tumour suppressors.

The Stenmark Lab studies the molecular mechanisms that promote or suppress cancer, a disease that involves uncontrolled proliferation and invasiveness of specific cell types of the body. Recently, his group has found that cells are equipped with an endogenous mechanism for lysosome repair which protects against lysosomal damage‐induced cell death, but which also provides a potential advantage for intracellular pathogens.

Lynda Stuart, Harvard Medical School, USA

Dr. Lynda M. Stuart earned an MD from the University of Cambridge and the University of London and a PhD from the University of Edinburgh in microbiological sciences and immunology.

In 2003 she joined the faculty at the Massachusetts General Hospital and Harvard Medical School where she was co-director of the Laboratory of Developmental Immunology; a member of the Center for Computational and Integrative Biology, an affiliate of the Broad Institute of Harvard and MIT; and served on the Massachusetts General Hospital Executive Committee for Research.

In 2016, Dr. Stuart joined the Bill and Melinda Gates Foundation where she leads the Vaccine and Host Pathogen Biology domain of Discovery and Translational Sciences. She also remains actively involved in basic research on innate immunity as an affiliate professor with the Benaroya Research Institute at Virginia Mason, Seattle.

David Underhill, Cedars-Sinai, USA

David Underhill got his Ph.D. in Cell Biology and Physiology from Washington University in St. Louis in 1995. Following postdoctoral training in innate immunity and macrophage biology at The Rockefeller University in New York City and the University of Washington in Seattle, Dr. Underhill joined the Institute for Systems Biology in Seattle in 2000 at its founding.

In 2005 he moved to Cedars-Sinai Medical Center in Los Angeles where he is currently a Professor in the Department of Biomedical Sciences, and the Janis and William Wetsman Family Chair in Inflammatory Bowel Disease Research. He was the founding director of the Cedars-Sinai Ph.D. Program in Biomedical Sciences and Translational Medicine and is a Professor-in-residence at UCLA.

Dr. Underhill’s work focuses on understanding how the body recognizes bacterial and fungal microbes in order to mount immune responses that are either inflammatory and protective against infection or tolerant and permissive to commensal microbes.

Maria Yurchenko, CEMIR, NTNU, Norway

Maria Yurchenko is a researcher in Trafficking group at CEMIR, Department of Clinical and Molecular Medicine at the Norwegian University of Science and Technology in Trondheim.

Maria is working together with Prof. Terje Espevik, and her research is focused on TLRs-mediated signaling, particularly TLR4-mediated signaling in human monocytes and macrophages. She is working on finding new targets for regulation of TLR4-mediated inflammation. Together with her colleagues in Trafficking group, she found novel interacting partners for TICAM2/TRAM adaptor protein (SLAMF1 and Rab11FIPs) that do not have TIR-domain and regulate TRAM intracellular trafficking and recruitment to TLR4.

Arturo Zychlinsky, Max Planck institute for infection biology, Germany

Dr. Zychlinsky is the director of the Department of Cellular Microbiology at the Max Planck Institute for Infection Biology in Berlin, Germany.

The Zychlinsky Lab boldly proposes that chromatin evolved to have an immune function in eukaryotes. This hypothesis is challenged by focusing on neutrophils and their ability to form structures while they are dying called Neutrophil Extracellular Traps (NETs).