Speaker
Description
Cancer is a complex, often tissue-specific disease that can lead to neoplastic outgrowth hallmarked by genetic, epigenetic, and microenvironmental factors. Tissue-disrupting tumors can occur when a population of somatic cells evolves within an organism. Adaptive tumor suppression involves the immune systems which can target pre-cancerous and cancerous cells for destruction. Compared to chemotherapy and radiotherapy, cellular immunotherapy modifies immune cells to induce the killing of tumour cells by humans’ own immune system. Cellular immunotherapy is effective due to direct killing of target cancer cells (prey) by immune cells (predator), such as specifically engineered T lymphocytes. Predator-prey dynamics is a modelling approach to mimic the dynamics between cancer and immune cells. Tumor growth is a sign of adaptation as cells that avoid killing gain higher fitness, leading to selection of seemingly resistant subtypes. We investigate the processes of T cell differentiation and killing assuming heterogeneity in T cell-target cell engagement. To this end, we consider the potentially stochastic and heterogeneous formation of conjugates of effector T cells and cancer cells, resulting in either cancer cell death or effector T cell inactivation. We capture the dynamics in small and large populations by applying stochastic and a deterministic birth-death and interaction dynamics. Our goal is to understand if and how effector cell-target cell conjugate dynamics play an important role in the evasion of cellular immunotherapy.
