Stavroula Piliou sp2046@cam.ac.uk
Greece
Pathology, Lucy Cavendish College
PhD thesis: Preventing and reversing neuroinflammatory brain damage in multiple sclerosis using local suppression
of the innate and adaptive immune system
Research interests:
- Neuroimmunology
- Autoimmunity
- Molecular biology
- Genetics
Multiple sclerosis is a chronic, unpredictable and often debilitating autoimmune disease during which the immune system attacks the myelin sheath that surrounds the nerve cells in the CNS, leading to symptoms such as fatigue, weakness, numbness and vision problems. While strides have been made in understanding neuroscience and peripheral inflammation, translating effective drugs into neuroimmunology is challenged by the blood-brain barrier and off-site immunosuppression concerns. My PhD project focuses on harnessing novel gene delivery tools to traverse this barrier, expressing anti-inflammatory and pro-repair biologics directly within the brain of preclinical mouse models. Through my research, I aim to explore the role of regulatory T cells in immunomodulation and remyelination, and unravel the intricacies of interleukins and cytokines in disease progression. My aspiration is that these insights pave the path for a revolutionary therapeutic, primed for clinical exploration and application.
Who or what inspired you to pursue your research interests?
I was inspired to pursue this project by the profound impact multiple sclerosis has on individuals' quality of life. Current treatments primarily manage symptoms rather than address the root cause. Recent research suggests that neuroinflammation plays a critical role in MS progression. By targeting and reversing neuroinflammatory brain damage through local suppression of the innate and adaptive immune systems, I hope to pave the way for novel therapeutic strategies. I believe that advancing our understanding in this area will open new avenues in the search for revolutionary neuro-immunotherapies, offering MS patients a life with fewer restrictions and more hope.