We pursue causes and mechanisms related to autoimmune diseases, with a central focus on rheumatoid arthritis and connective tissue diseases like SLE. It is our aim to improve the understanding of basal mechanisms, leading to solutions that will offer precision health and not only precision medicine.

Infection of the airways of the lung leads to a powerful inflammatory response, which impairs their ability to exchange CO2 and O2 effectively, as this is highly dependent on the integrity of the delicate anatomical structures. Our vision is to identify factors and signalling pathways that are important for limiting inflammation induced pathology in the lung during infection.

Our research aims at deciphering the molecular mechanism of autophagy, with also a focus in understanding the role of this pathway in preventing neurodegeneration and regulating immunity. In this latter context, we are investigating the unconventional functions of autophagy-related proteins in controlling viral infections

Immunosurveillance is an essential function of the immune system to protect the body against bacteria and viruses. It participates in controlling self-host damage responses and development of cancer and autoimmune diseases. We explore questions in context of viral infections, inflammation and cancer, from both a basic science and clinical translational angle.

See also JAKOBSEN research group

My lab studies the processes creating inflammation in the body, resulting from infections, autoimmune diseases and damages after surgeries. I focus on the role of pattern recognition molecules, which can differentiate between the body's normal proteins, and the pattern of ligands on the surface of a number of micro-organisms or stressed cells.

We investigate the function of macrophages, macrophage polarization and role of macrophage scavenger receptors acute/chronic inflammatory conditions including in the tumour immune-microenvironment. One major goal of our group is to transform our findings into novel therapeutic strategies.

We are interested in understanding how the innate immune system senses infections and sterile damage and how this impacts disease pathogenesis. To achieve this goal we use a broad range of methods ranging from molecular biology and molecular genetics, via cell culture systems to animal models.
See also Paludan lab 

We investigate molecular mechanisms in chronic inflammation and autoimmune diseases to understand and design new biological therapies. Our interests also include antimicrobial peptides with a view to develop new antibiotics from drug repurposing to counter resistance to classic antibiotics.

Our focus: Genetic and immunological basis of viral infections in humans. We perform genome sequencing on DNA from patients, followed by immunological characterization of patient cells. This leads to new understanding of molecular mechanisms underlying primary immunodeficiencies and increased susceptibility to infectious diseases.
See also research group website

Associate Professors

Our research focuses on understanding the function of distinct macrophage subsets in progression of cancer and chronic inflammatory conditions. To realize this, we utilize a wide range of methods, including single cell transcriptomics, whole tissue imaging, antibody-drug targeting and murine models.

Our research group studies structural and functional aspects of receptors involved in infection and inflammation. Current projects focus on the human haemoglobin scavenger receptor CD163 and the S. aureus iron-regulated surface determinant system.

Our research focuses on the understanding of the early events involved in the host response to oncolytic and emerging virus infection, with the long-term objective to utilize the knowledge of the host response against virus infections to develop novel therapeutic approaches for the treatment of resistant cancers and viral diseases.

Our research is focused on various aspects of cardiometabolic disease, ​with a special interest in inflammatory resolution. We investigate specialized, pro-resolving lipid mediators, such as lipoxins, and their ability to promote cardiometabolic health in obesity. We combine experimental studies with basic clinical research.

Our team investigates the role of human skin bacteria. Major projects are: (I) discovery and investigation of bacterial species associated with hospital-acquired and implant-associated infections; (II) mechanistic understanding of the role of bacteria in skin disorders and skin health.
See also:

Impaired vascular remodeling during the expansion of adipose tissue increases the rates of cardiovascular disorders (CVD). In order to understand obesity-mediated CVD, we use multidisciplinary approaches (scRNA-seq; proteomics) to explore the heterogeneity of adipose endothelium and its dysfunction.
See also Kalucka-lab

CNS inflammation is a common hallmark in several CNS diseases. We investigate the role of protective immune reactions and harmful inflammatory responses by studying interactions between glial cells and neurons in their organization of antiviral responses, inflammation, and cell death.

The infectivity of several pathogenic bacteria is tightly associated with biofilm formation mediating resistance to host immune response and antibiotics. The structural component of biofilms is functional bacterial amyloids (FuBA). Our research activities are focused on understanding the molecular mechanisms involved in the formation of FuBA.

My research group aims to study cancer in advanced animal models by use of CRISPR technology. We use a mini-pig expressing Cas9 and a similar mouse model. The cancer is induced by AAV expressing CRISPR guides. We are currently focusing on glioblastoma, prostate and lung cancer in these models.

We study mechanisms promoting the dissemination of melanoma cancer. Focus is the characterization of key membrane receptors, endolysosomal compartments and central signalling pathways at different differentiation stages. In connection with this, we study melanoma communication and cooperativity with immune cells.

Translational research: pathogenesis of Multiple Sclerosis (MS) and NeuroMyelitis Optica Spectrum Disorders (NMOSD): neurodegeneration and inflammation; biomarkers; immune cell subsets; epigenetic regulation; involvement of Human Endogenous Retroviruses (HERVs) and HERV-related pathogenesis.

Our research is focused on immune mediated inflammatory diseases with special interest in arthritis. Based on unique human ex vivo models of arthritis projects include both very basic research studies trying to identify new pathogenic mechanisms and translational studies of biomarkers and drug pharmacodynamics.

We focus on the role of B and T lymphocytes in health and disease, with a particular emphasis on tolerance and autoimmunity. Lymphocytes display the remarkable abilities of ‘learning’ and ‘memory’. We investigate these phenomena in mouse models using molecular tools, cytometry and microscopy.

Cellular responses are orchestrated by cells exerting diverse functionalities. Cellular heterogeneity is prominent, particularly in immune-related contexts and even seemingly similar cell groups. Our vision is to advance the analysis of and exploit the differences within cellular functionalities of individual immune cells for therapy, diagnosis and personalization.

We study infections in pregnancy and early life, evaluate transplacental transfer of different antibodies and antibiotics and protection in neonates. With a specific focus on Streptococcus agalactiae, we investigate sepsis and meningitis in early life.

Assistant Professors

Our research focuses on understanding how unique interactions between immune cells and muscle stem cells orchestrate effective muscle regeneration, and on investigating whether these interactions are impaired during ineffective muscle regeneration, in aging and muscular dystrophies. See also: Porpiglia-lab

We study the rewired metabolism of pancreatic cancer cells and their crosstalk with the tumor microenvironment. We use a multi-disciplinary approach including metabolomics/proteomics and animal models. We aim to identify novel metabolic vulnerabilities that can be targeted with available drugs.

STING is a master regulator of immunity and plays important roles in various disease contexts. However, STING overactivation can lead to excessive inflammation, which can aggravate a wide range of pathologies such as autoimmune or neurodegenerative diseases. We study the molecular and cellular mechanisms of STING activation and regulation.

The immune response to viral infection may cause much greater damage than the virus itself. Studying patient specific gene variants in transgenic mouse models of Herpes Simplex Encephalitis, we explore how the innate immune system senses virus in the brain, mounts a tightly regulated response, and deciphers the molecular mechanisms underlying disease development.