Ingunn Stromnes Lab - Graduate Student Research

Eduardo Cruz

Eddie is researching the role of CD4+ T cells in mediating anti-tumor immunity after immune checkpoint blockade. By using a MHC-II tetramer, Eddie is tracking changes in the polarization of CD4+ T cells as tumors progress to identify how CD4+ subsets are responding to therapy. Eddie's research also makes use of immunofluorescent techniques to characterize the spatial cell-to-cell interactions associated with immunotherapy response and tumor control. Future directions include characterizing CD4+ T cell function and exhaustion in pancreatic cancer.

Cara-Lin Lonetree

My research focuses on genetic engineering of CD8 T cells for novel and effective treatment of pancreatic cancer. CD8 T cells are a crucial component of the immune system that fight off foreign viruses and bacteria, as well as our own cells that have become cancerous. While pancreatic cancer is very good at shutting down the T cells that have made their way into tumors, decades of research have enabled us to manipulate T cell DNA in ways that may improve their functionality and persistence in the solid tumor microenvironment (TME). I am engineering tumor-specific T cells to continuously produce different signaling molecules called cytokines and screening for improved T cell fitness, potential TME remodeling, and other beneficial effects in the Stromnes Lab’s pancreatic cancer mouse models.

Grant Hickok

My current thesis proposal concerns the immune response elicited by immune checkpoint blockade (ICB) therapy against pancreatic cancer. Specifically, I am interested in the role that TCR affinity plays in the functionality of newly recruited "stem-like" CD8 T cells (CD8STEM). CD8STEM cell possess a high self-renewal potential and form reservoirs in both tumor draining lymph nodes and tertiary lymphoid sites within the TME, continually supplying cytotoxic effector cells to the anti-tumor response. It has been shown in other cancer models that CD8s presenting TCRs with low tumor epitope affinity have been found to comprise the majority of this CD8STEM reservoir when in competition with CD8s expressing high affinity TCRs. However, this lower affinity CD8STEM population exhibits reduced functionality and does not benefit from ICB. Understanding what causes low affinity TCRs to comprise the CD8STEM reservoir in models of competition, as well as how to potentially rescue dysfunctional CD8STEM, could help improve the longevity and potency of the ICB mediated response to pancreatic cancer.