Biography
Peter Draber received PhD in immunology from Charles University in Prague in 2011 under the guidance of Tomas Brdicka. His thesis focused on analyzing novel transmembrane adaptor proteins regulating immune signaling. Subsequently, in 2012, he joined Henning Walczak's laboratory at University College London as a postdoctoral scientist. There, he studied the regulation of cell death induction and its role in autoinflammatory diseases. In 2017, Peter joined Ondrej Stepanek's group at the Institute of Molecular Biology in Prague to focus on T cell development and the regulation of adaptive immune responses. Building on these research experiences from various fields of immunology, in 2020, he established a new research group at the BIOCEV research campus in Vestec, Czech Republic. He searched for new components of several cytokine receptors. In January 2024, Peter was appointed tenure track Assistant Professor at the Department of Immunobiology at the University of Lausanne. His current research is dedicated to uncovering new therapeutic targets to modulate the immune responses
Research Interests
The immune system has evolved to defend the organism from invading pathogens and to remove infected and mutated cells. At the same time, regulatory mechanisms have been established to keep immune tolerance towards the host. The inability to properly regulate immune responses underlies many autoimmune conditions that can severely impact the quality of life. A detailed understanding of how immune balance is established might lead to new therapeutic approaches to restore immune homeostasis in pathological conditions.
Draber laboratory aims to discover new major regulators of immune responses and identify potential therapeutic targets to modulate the immune system in disease settings. For that purpose, the research is divided into three complementary areas.
Research Area 1. Identification of new regulators of cytokine signaling. Cytokines are small proteins guiding proper immune responses but can also drive severe autoimmune disorders. For example, IL-17 is critical to protect the host from yeast infections but is strongly implicated in psoriasis. Similarly, TNF is crucial to mount an immune response against invading pathogens, but it also promotes various autoimmune disorders such as rheumatoid arthritis or inflammatory bowel disease. The research goal is to employ mass-spectrometry analysis of important cytokine receptors to identify new regulators of their signaling that might eventually be targeted for immunomodulation.
Research Area 2. Search for new pathways regulating programmed cell death in vivo. The group established a new model of TNF-mediated autoimmunity by preventing the recruitment of kinase TBK1 to the TNF receptor 1 signaling complex, which strongly potentiates TNF-induced cell death. This model can help to elucidate new pathways to suppress autoinflammation and restore immune balance. Aberrant cell death accompanies various autoimmune diseases. Therefore, finding new venues to block cell death-inducing pathways might lead to new treatment options for alleviating certain autoimmune disorders.
Research Area 3. Analysis of the role of regulatory T cells (Tregs) in the protection from programmed cell death. The group recently developed the hypothesis that Tregs might directly protect from programmed cell death, independently of their role in regulating conventional T cells. This would represent an entirely new function of Tregs. The proposed research aims to connect two scientific fields currently studied separately: induction of extrinsic cell death and regulation of adaptive immune responses. This work might provide a new understanding of how immune homeostasis is established.
