Utilizing the Multi-parameter Capability of the ZE5 to Monitor T-Cell Exhaustion Following Immunotherapy.

Abstract

Abstract The immune systems as evolved sophisticated mechanisms to distinguish between self and non-self, and dangerous and non-dangerous signals leading to appropriate and controlled immune responses against infection and cancer or tolerance to avoid attacking the host body. One pathway of immune suppression is T-cell exhaustion which shuts down effector T-cells. T-cells or T-lymphocytes, are an immune cell that help protect the body from infection and fight cancer. T-cell exhaustion is exploited by chronic viral infections and cancers to escape being targeted by the immune system. It results in a sustained expression of suppressive cell surface markers and effector function in these cells, meaning they are no longer able to function to remove the cancerous and infected cells. Recently, researchers have focused on using monoclonal antibody drugs to block these suppressive cell surface markers and re-invigorate the T-cells, restoring their effector capability to clear viral infection and cancer cells from the body. In this study, we use a 15-parameter panel to examine in-depth changes to the T-cell phenotype, exhaustion and cellular subset identity markers before and after chronic stimulation and in combination with a monoclonal antibody drug treatment targeting the receptor Programmed Cell Death 1 (PD-1).