Chronic inflammatory skin diseases with high prevalence such as psoriasis, atopic dermatitis, or lichen planus exemplify how failure of tissue-resident immune regulation can lead to distinct immune response patterns. These skin diseases are manifestations of specific cytokine-driven inflammatory endotypes, commonly referred to as Type 1 (T1; e.g. lichen planus), Type 2 (T2; e.g. atopic dermatitis), Type 3 (T3; e.g. psoriasis), and Type 4 (T4) immune diseases. Type 4 inflammation includes fibrosing (T4a) and granulomatous (T4b) patterns that are relevant for diseases such as morphea and cutaneous sarcoidosis. Understanding the cytokine signaling signatures underlying these diseases offers not only diagnostic precision but also enables rational therapeutic selection. This project integrates cytokine profiling into the framework of skin health and resilience, supporting the overarching goal of the graduate college to define molecular pathways of health, early immune deviation, and preventive intervention.
Our research group focuses on the complex interactions between immune cells and kidney epithelial cells. By analyzing cells found in urine, examining kidney biopsy samples, and utilizing cell culture models, we aim to gain deeper insights into the mechanisms underlying kidney injury and repair. Our work centers on the study of human patient samples, allowing us to address the fundamental question of how kidneys are damaged during disease and how they recover following injury.
The goal of my laboratory is to understand the regulation and control mechanisms of immune responses at barrier sites. Barrier sites such as the lungs are continuously exposed to the environment and potential entry ports for pathogens. A unique network of cell populations ensures appropriate immune responses to defend the body against potential pathogens but also to maintain organ function and health at steady state. However, the underlying mechanisms are poorly understood. Group 2 innate lymphoid cells (ILC2) are tissue resident and able to secrete large amounts of cytokines within a short time period and thereby orchestrate innate but also adaptive immune responses. Thus, studying the regulatory processes of ILC2 effector function is key to understand immune concepts of immunity and health at barrier sites.
The scientific focus of our lab centers on unraveling the multifaceted role of clonal hematopoiesis (CH) in disease prevention and inflammatory processes. CH is recognized as a pre-malignant condition that significantly increases the risk of hematologic malignancies. Beyond its oncogenic potential, CH has emerged as a critical risk factor for cardiovascular diseases such as stroke, myocardial infarction, and atherosclerosis, contributing to both initial and recurrent events. Moreover, CH is intricately linked to chronic inflammation, functioning both as a driver and a consequence of sustained immune dysregulation. By investigating these complex interconnections, our research aims to deepen the understanding of CH as a central node in disease pathogenesis and to identify novel strategies for early intervention and prevention.
Sulfate is an essential nutrient that supports numerous biological processes, including tissue development, cellular function, and overall physiological homeostasis. Its concentration in the body is tightly regulated by specialized sulfate transporters that mediate both dietary absorption and renal reabsorption. Despite its fundamental roles, the contribution of sulfate to vascular biology has been largely overlooked. Emerging evidence suggests that sulfate is critical for maintaining the structural and functional integrity of blood vessels, particularly through its incorporation into sulfated glycosaminoglycans, which are key components of the endothelial glycocalyx. We hypothesize that sulfate plays a vital role in preserving vascular integrity, supporting endothelial function, and regulating blood flow-domains that remain underexplored and represent significant knowledge gaps in biomedical research.
Are you passionate about scientific questions related to understanding the basis of health and disease? Are you interested in applying your findings to answer clinically relevant questions for molecular prevention and the development of novel therapies?
An update on further recruitment rounds will follow shortly.
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Our group aims to understand the molecular mechanisms involved in tissue homeostasis, inflammation, and resolution of inflammation. Our main focus is on the transcription factor NF-κB and its role in the intestinal epithelium. Our current projects range from determining the role of the transcription factor in epithelial regeneration in colitis and in inflammatory bowel diseases (Re-Thinking Health, 2022), to refining analgesia (Charité 3R), to investigating the role of NF-κB in cellular senescence in the gut (DFG) or its role in metabolism.
Our research aims to understand the role of tissue-resident cells of the innate immune system in the prevention of chronic inflammatory diseases such as systemic lupus erythematosus and inflammatory bowel disease. Our goal is to identify mechanisms that may inhibit the transition from homeostasis to chronic inflammatory disease and to determine the role of tissue-resident cells of the innate immune system in this process. Understanding such mechanisms may allow to answer the question of why some patients are susceptible to chronic autoimmune-related inflammatory diseases and others are not, and how to improve/achieve resistance to chronic inflammatory diseases.
In our project, we focus on maladaptive immune responses to prevent multi-morbidity in patients with chronic kidney disease (CKD). Based on our longstanding interest in microbiome-immune interactions in cardiovascular and renal diseases, the planned project involves first proof-of-concept clinical studies side by side with experimental in vitro assays. Our translational project addresses a molecular mechanism that is crucial to maintain health and opens up areas for preventative strategies in line with the Re-thinking health program.
The gastrointestinal epithelium is organized into clonal crypts that represent sophisticated anatomical and functional tissue units. The epithelium is intimately associated with the mesenchymal stroma network, and various mesenchymal cell types are essential constituents of the stem cell niche that regulates epithelial homeostasis. The gastrointestinal stem cells give rise to differentiated cells. This process is important to maintain the nutritive absorptive functions of the epithelium as well as to build a barrier against pathogens and toxins from the environment. Recently, it has become increasingly evident that interactions between the epithelium and stroma are vital in regulating the barrier function, allowing tissue adaptations to environmental perturbations1,2. Our research aims at understanding the interplay between the epithelium, stroma and the microbiota. We would like to understand how tissues respond to microbiota alterations or exposure to pathogenic bacteria as well as their toxins. To address this, we are also developing new organoid and assembloid models to recapitulate the cellular networks observed in vivo.
Diabetics have a higher risk of various infectious diseases including pneumonia. Current estimates suggest that 450 million people worldwide have diabetes, and this number will increase to approximately 700 million by 2045. The increase in diabetes prevalence is thus likely to cause an increase in pneumonia-related morbidity and mortality. A better understanding of the mechanisms underlying diabetes-related dysregulation of the antibacterial immune response may allow to develop more targeted prophylactic strategies to prevent pneumonia in diabetic individuals.
The airway mucosa represents the first line of defense of the respiratory system against pathogens, pollutants, and irritants that are constantly inhaled during tidal breathing. Elimination of these potentially harmful stimuli by mucociliary clearance is an important innate defense mechanism of the lung, which operates through the coordinated function of (i) the motile cilia, (ii) the airway surface liquid layer, and (iii) the mucus layer.
Acute respiratory distress syndrome (ARDS) is a serious complication of infectious or sterile lung inflammation, typically as a consequence of pneumonia or sepsis, with high morbidity and mortality (30%-40%) and presently no pharmacological or mechanistic treatment strategies. This critical knowledge and treatment gap became strikingly evident in the recent COVID-19 pandemic, with ARDS as the main cause of death1,2. ARDS is characterized by a breakdown of the lung vascular barrier and the leak of fluid from the blood into the airspaces, preventing normal lung mechanics and gas exchange. Traditionally, mechanisms of ARDS are studied in animal models, which have, however, translated poorly into the clinical scenario. Here, we will assess mechanisms of lung vascular barrier integrity and regeneration in a novel microphysiological Microvasculature-on-Chip (MOC) model that allows to track vascular morphology and leak as well as the dynamics of individual cell types and their interaction in an unprecedented temporal and spatial context. Here, we will employ this model for the first time to study lung vascular barrier integrity, and to devise strategies for its maintenance in experimental settings mimicking ARDS.
Sulfate is an ion that is indispensable for human health. It is necessary for the formation of connective tissues, including bone and cartilage. The kidney plays a central role in body ion homeostasis by reabsorbing electrolytes from the tubular fluid. Specifically, the proximal tubule is a major site for fluid, protein, and nutrient retrieval. Our working groups recently described a patient who presented with unexplained chronic chest pain and a kidney stone.
Our group is interested in identification and investigation of genetic, clinical, and environmental factors determining onset of chronic kidney disease (CKD) and kidney survival. We make use of next-generation sequencing techniques and deep-phenotyping to identify genetic variants that are predictive for disease progression or convey protection from organ failure. We functionally evaluate identified germline variants in vitro in order to understand underlying molecular mechanisms leading to CKD on the one hand or protecting from kidney failure on the other. By doing so, we aim at defining and targeting molecular switches responsible for health maintenance and disease alleviation.
We study development and function of the innate immune system, in particular of innate lymphoid cells (ILC). A current focus is to obtain a molecular understanding of how the innate immune system, by integrating environmental signals (such as those derived from nutrients, microbiota, circadian rhythm) contributes to tissue physiology. Recent studies have revealed ever more intriguing relationships between innate immune system components and basic developmental and biologic processes that are