Spring 2023 Recipients

The immune system plays a critical role in regulating tumor growth by enabling T cells to selectively recognize and kill tumor cells, leading to the development of immunotherapy, such as immune checkpoint inhibitors (ICI). However, T cells are vulnerable to the effects of aging, which can result in a decline in their development, maintenance, and function. Despite the significance of this issue, the impact of aging on anti-tumor immunity and response to ICI remains unclear. As a post-doctoral fellow in Drs. Marcia Haigis and Arlene Sharpe's labs, my primary research focus is to understand how anti-tumor T cell immunity declines with age and the metabolic mechanisms that facilitate this process. My long-term goal as an early-career scientist is to unravel the complex mysteries of how our immune system deteriorates with age, its implications in age-associated chronic illnesses, and develop rational therapies targeted towards reversing the effects of aging on our immune system.

My broad research interest is understanding how mammalian cells tune protein localization and remodel the proteome in response to a myriad of cellular stress conditions through protein production, transport, and degradative mechanisms. One such pathway involves autophagy-dependent degradative mechanisms that remove superfluous or damaged organelles and proteins to allow recycling of building blocks for cellular remodeling. Macroautophagy during nutrient stress has long been considered to result in non-specific capture of bulk cytoplasmic contents within autophagosomes. However, recently we combined quantitative proteomics with a computational pipeline that deconvolutes starvation-based cellular responses. Through this analysis, we found that selective forms of Endoplasmic Reticulum and Golgi Apparatus degradation by autophagy is “hard- wired” into a broad autophagic response to nutrient stress. We are now working to uncover molecular factors and mechanisms involved in specific organelle remodeling by macroautophagy.