Stress Response and Metabolic Reprogramming in the single cell era

The intricate interplay between metabolism, stress, and epigenetics in immune cells plays a pivotal role in the pathogenesis of diseases such as Glioblastoma and Sepsis. My external seminar will explore how metabolic reprogramming and epigenetic modifications influence immune cell function in these diseases, with a focus on myeloid cells. Leveraging advanced single-cell technologies, we are investigating how these internal and external cues shape immune responses, and whether these changes are present in immune cell precursors.
I will introduce novel tools developed by our team to study metabolism and epigenetics at single-cell resolution in patient samples, aiming to shed light on the early immunometabolic states that dictate long-term immune responses. These innovative platforms, including SCENITH™ and its expantion into the spatial and epigenetics fields enable detailed metabolic profiling with spatial and multi-omic potential at the single-cell level, offering new insights into cellular function within the tumor microenvironment and septic conditions.
In addition, I will present SNUPR, a cutting-edge methodology designed to profile the unfolded protein response (UPR) and predict therapeutic responses to Bortezomib in patients with multiple myeloma. SNUPR holds promise for improving patient outcomes by identifying biomarkers that can guide personalized treatment strategies.
By integrating spatial, multi-omics, and single-cell technologies, our goal is to translate these discoveries into clinical applications, improving diagnostic precision and therapeutic interventions in cancer and sepsis. The findings I will discuss represent a step forward in understanding immunometabolism and its implications for trained immunity in both pediatric and adult patients, ultimately aiming to bridge the gap between fundamental research and clinical impact.