Interview – Dr Monica Schaller Tschan
Context
On January 5, 2026, Dr. Monica Schaller Tschan held a seminar at the School of Biotechnology for the UMR, organized by Prof. Sylviane Muller, entitled: “What is our contribution to understanding the dysregulated autoimmune response in iTTP – where do we go from here.” We were able to gather her testimony as well as a short editorial recounting her career and her perspectives in the world of research.
Dr Monica Schaller Tschan editorial
As a molecular immunologist with extensive experience in the field of autoimmune diseases, my work aims to elucidate the pathophysiology of autoimmune diseases in the broadest sense, with a particular focus on thrombotic thrombocytopenic purpura and related autoimmune thrombotic diseases. The main thread running through my entire scientific career has been the use of my expertise in cloning autoantibody repertoires as tools for the development of new therapeutic approaches. I have thus contributed to the development of innovative strategies targeting autoantibodies directed against glucose-6-phosphate isomerase (GPI) in patients with autoimmune rheumatoid arthritis (Schaller et al., Nature Immunology, 2000), against C1q in patients with systemic lupus erythematosus (Schaller and Bigler et al., Journal of Immunology, 2009), and against ADAMTS13 in patients with iTTP (Schaller et al., Blood, 2014).
My current research interest is to explore the autophagy–NET axis as a central driver of pathogenic inflammation and an innovative therapeutic target in thrombotic autoimmune diseases, with a particular focus on immune-mediated thrombotic thrombocytopenic purpura (iTTP; Figure 1). Although the formation of extracellular neutrophil traps (NETs) plays a protective role when finely regulated, excessive release or defective clearance of NETs becomes pathogenic. In this context, extracellular DNA and neutrophil granule proteins act as autoantigens and potent inflammatory stimuli, promoting autoimmunity and thrombosis (Buonomo et al., submitted). As an upstream regulator of NET formation and clearance, autophagy contributes to NET-induced platelet activation, microvascular thrombosis, and disease severity in immune-mediated thrombotic disorders. By systematically evaluating the deregulation of autophagy and NET formation, I aim to identify therapeutic strategies capable of disrupting the autophagy-NET-inflammation axis and restoring immune homeostasis.
It is in this context that I am particularly delighted to have been invited to visit you, in order to strengthen our collaboration in doctoral training, in my capacity as coordinator of the doctoral program in biomedical sciences at the University of Bern, and to expand this collaboration into a closer scientific partnership.
Interview
What were the key steps in your scientific career that led you to work on immunology and autoimmune diseases?
My scientific career has gradually developed around molecular immunology and autoimmune diseases, with several key milestones:
- Initial training and PhD in molecular biology, which gave me a foundation in cellular and immune biology.
- International postdoctoral fellowships in leading laboratories (TSRI La Jolla, University of Basel, then Inselspital Bern), where I further developed my skills in immunology and autoimmunity.
- Habilitation (Venia Docendi) in immunohematology, consolidating my ability to lead independent projects.
The focus on autoimmune diseases remains a common thread: I first studied autoantibodies in rheumatoid arthritis, then in systemic lupus, before concentrating on autoimmune mechanisms in rare diseases such as immune-mediated thrombotic thrombocytopenic purpura (iTTP).
How would you summarize the main objectives of your current research?
- Understanding the genesis and evolution of the dysregulated immune response that leads to the production of autoantibodies in various autoimmune diseases.
- Using human autoantibodies as tools to identify new therapeutic targets, in particular through antibody repertoire cloning.
Develop innovative therapeutic strategies that specifically target the pathological components of the dysregulated immune system (e.g., anti-idiotypic molecules (DARPIN) to neutralize autoantibodies).
In summary, the goal is to move from mechanistic understanding to targeted interventions that can improve clinical management or diagnosis.
Your team is developing new approaches: how could these advances transform future patient care?
- Targeted therapies against pathogenic autoantibodies: for example, we generate small anti-idiotypic molecules (DARPins) capable of neutralizing the autoantibodies responsible for ADAMTS13 deficiency in iTTP, which could restore enzyme activity and prevent microthrombus formation.
- Immunological biomarkers: Autoantibody genotypes could help better predict disease progression, risk of relapse, or response to treatment.
- Understanding dysfunctional intracellular mechanisms (such as aberrant autophagy and NET formation in immune cells) could pave the way for new classes of immunomodulatory treatments.
These approaches could reduce dependence on non-specific immunosuppressive treatments, decrease adverse effects, and improve patients’ quality of life.
What challenges did you encounter and how did you overcome them?
Scientific research faces several challenges:
- The complexity of autoimmune diseases: their etiology is multifactorial and unpredictable, requiring sophisticated experimental models and interdisciplinary collaboration.
Solution: build a strong network of national and international collaborations to pool expertise and technologies. - The study of this rare disease is particularly complex and, in the absence of an animal model for iTTP, access to a sufficient number of samples is a major challenge. Solution: Longitudinal approaches in patients, allowing the analysis of paired samples taken at different stages of the disease (acute phase, response to treatment, remission), with each patient serving as an internal control. This is possible with our established multicenter biobanks.
- Competitive funding for transnational projects.
Solution: Apply for various academic and integrated funding programs (SNSF, IMS, public-private partnerships).
Perseverance, adaptability, and teamwork have been essential in overcoming these obstacles.
You have received several awards, including a prize at the GTH 2022: what do these awards mean to you in your career as a researcher?
The GTH 2022 poster award recognizing my work on immune responses to ADAMTS13 is an important validation of the scientific quality and translational impact of my research and a step towards development.
These distinctions:
- enhance the visibility of the laboratory and facilitate the development of future collaborations and funding.
- are a source of personal and professional motivation to pursue innovative approaches.
As director of a Graduate School (GCB), what skills do you think are essential today for training the next generation of researchers?
Here is a selection of skills that I consider essential:
- Scientific critical thinking: ability to analyze and interpret large amounts of data.
- Interdisciplinary skills: integrating approaches from biology, immunology, bioinformatics, etc.
- Communication and collaboration: working effectively in international teams.
- Research ethics: understanding of ethical, regulatory, and social issues related to science.
- Project management and leadership: planning, managing resources, and leading teams.
These skills enable you to be not only a good researcher, but also a scientific leader.
What advice would you give to current and future researchers?
- Cultivate scientific curiosity and remain open to new ideas and technologies.
- Share your results and thoughts: science progresses through transparency and exchange.
- Develop personal resilience: research involves failures before successes.
- Stay focused on the clinical or societal impact of your work, especially in biomedical sciences.
Thanks so much to Monica Schaller Tschan for agreeing to this interview!
