Angie Green, Chris Brampton, Kristin Lind, Matt Alexander, Yasha Talaga, and Elizabeth Dreskin Bio-Rad Laboratories, Inc., Hercules, CA 94547 USA

The immune system has evolved sophisticated mechanisms to distinguish between self and nonself, and dangerous and nondangerous 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 are immune cells 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 reinvigorate the T cells, restoring their effector capability to clear viral infection and cancer cells from the body.

In this study, we use a 16-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 programmed cell death protein 1 receptor.