Abstract
Abstract Radiation therapy (RT) is a pivotal component of cancer treatment, yet its impact on the immune system is not fully understood. RT induces DNA damage in cancer cells, promoting cancer cell death and RT-induced immune responses with the potential to clear surviving cancer cells. However, RT can also recruit suppressive T regulatory cells (Tregs), that hinder adaptive immunity. Following RT-mediated death of tumor Tregs, we hypothesize that immature Tregs are recruited to the post-RT tumor and converted into suppressive phenotypes. Using the Kaede mouse model, we tracked photoconverted cells from either the tumor or TdLN after RT. In photoconverted tumors, Tregs in the TdLN constituted a higher proportion of photoconverted cells compared to non-Treg CD4 or CD8 T cells. When RT was applied to tumors, photoconverted Tregs and non-Treg CD4 T cells decreased in the TdLN. When photoconverting the TdLN we observed selective migration of Tregs to the tumor rather than to NdLN. Analyzing these newly arrived photoconverted Tregs in the tumor post-RT revealed increased expression of CD69, KLRG1, and Ly6C compared to non-photoconverted Tregs, indicating limited suppressive capacity. Ongoing studies are examining the impact of the irradiated tumor environment on newly-entered Treg plasticity. These findings unveil intricate dynamics between RT, Tregs, and the use of site-specific photoconversion for tracking immune cell movement over time.
Published Version
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