Ben Capozzoli

I am a graduate student in the Bamezai lab studying the ability of the immune system to fight cancer. Current trends in the biotechnology and pharmaceutical world are investigating the immune system more frequently as a viable option for cancer therapies so a growing number of proteins are being identified that regulate the immune response to a tumor. Previously, work from the Bamezai laboratory has demonstrated that the protein Ly-6A negatively regulates T cell clonal expansion when the T cells are stimulated (Henderson et al. 2002 and Lang et al. 2017).

How exactly Ly-6A does this is still unknown, but what we do know is that cell divisions are significantly reduced during in vitro experiments where cells over-express Ly-6A (Henderson et al. 2002). Similarly, cells that have Ly-6A stimulated in vitro have been shown to undergo cell death more often as well as divide less often even when simultaneously receiving a stimulus that should cause cell divisions. This could indicate that Ly-6A belongs in a growing family of proteins called immune checkpoint inhibitors that includes notable pharmaceutical successes like PD-1 and CTLA-4. As I have highlighted, what we know about Ly-6A so far has been demonstrated in vitro, so my project attempts to demonstrate the seemingly inhibitory qualities of Ly-6A in vivo. To do this I am using a cancer model where mice lacking Ly-6A or with Ly-6A blocked with and antibody to see if this is enough to cause the mice to successfully fight the tumor. A number of proteins are also being shown to more effective in synergy with proteins like PD-1 than they are on their own, so I also am attempting to investigate that relationship as well and determine if such a synergy between Ly-6A and PD-1 does exist.