Wladislaw Stroukov
Academic and Work Experience Prior to Sept 2018 Programme Start
I completed my undergraduate degree in Molecular Medicine and a master’s degree in Biochemistry and Biophysics at the Albrecht Ludwig University of Freiburg.
PhD Programme – Year 1 – MRes and Project Rotations
During my first rotation project I worked with Dr. Francesca Spagnoli focussing on the in vitro generation of insulin-secreting pancreatic β-cells from human pluripotent stem cells.
During my second rotation I joined Dr. Shukry Habib’s group and investigated the early signal recruitment of mouse embryonic stem cells in the context of self-renewal.
In my final rotation I worked with Prof. Giovanna Lombardi and Dr. Cristiano Scotta and investigated the phenotype and function CD101+ regulatory T cells in patients with systemic lupus erythemasosus.
PhD Programme – Years 2 to 4 – Doctoral Studies
Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disorder primarily affecting women between early adolescence and menopause. Characteristic for SLE is the dysregulation of the immune system leading to systemic inflammation and tissue damage. Regulatory T cells (Tregs) which suppress excessive immune responses lose their ability to appropriately suppress other immune cells. Analysis of the transcriptional signature in Tregs identified markers that might be involved in disease progression. One of the identified markers is the surface protein CD101 which is present on highly suppressive Treg subsets in mouse models and patients with active SLE exhibit a near complete loss of this subpopulation.
With this project, we propose a multi-faceted approach of phenotypic and functional characterisation of CD101+ Tregs in established cell culture assays and mouse models to validate their suitability for potential adoptive cell therapies. High-dimensional analysis will provide a personalised deep- phenotypic and transcriptomic signature of immune cells and correlate these data to disease progression. Thus, delivering a detailed profile of the subset distribution of Tregs and other cell types affected by the loss of Treg function in SLE. Thereby, we aim to provide detailed insights into the pathophysiology of this heterogeneous disease and identify potential diagnostic markers that facilitate patient-specific therapeutic decisions.
