Investigating Mechanisms of Action (MOA) of Anti-PD-1 Treatment by Systematic Depletion of Different Immune Cells in Syngeneic Models
Ying Jin, Jan Muntel*, Haochen Yu*, Kristina Beeler*, Roland Bruderer*, Yongli Shan, Annie Xiaoyu An, Davy Xuesong Ouyang, Henry Qixiang Li
*Biognosys AG, Zurich, Switzerland
To optimize immune checkpoint inhibitor use it’s important to fully understand which immune cell populations mediate response. For example, while it’s well known that anti-PD-1 antibodies work via activation of cytotoxic T cells, the contribution of other immune cell populations are not well defined.
To understand how different immune cell lineages impact anti-PD-1 efficacy, we combined anti-PD-1 treatment with different immune cell population depletion in MC38, CT-26, EMT6, and Hepa 1-6 murine syngeneic models. Proteomic analysis was also performed on tumor samples from selected MC38 and Hepa 1-6 model subgroups.
Read this Poster to Discover:
- That CD8+ T cell depletion severely weakens or completely diminishes anti-PD-1 efficacy, while CD4+ T cell depletion induces contrary effects across models
- How proteomic data analysis uncovers part of the MOA leading to differences in CD4 depletion between MC38 and Hepa 1-6 models
- How immune cell lineages act differently upon anti-PD-1 blockade release dependent on specific tumor microenvironments