The checkpoint inhibitor TIGIT limits antitumor and antiviral CD8⁺ T cell responses

Abstract

Success in eliciting tumor rejection by therapeutic blockade of T cell checkpoint inhibitors, such as PD-1/PD-L1 and CTLA-4, has spurred re-evaluation of additional receptors that regulate antitumor responses. Here we summarize our recent studies characterizing the role of co-inhibitory receptor TIGIT in antitumor and other chronic CD8⁺ T cell responses.

Keywords:

• TIGIT
• CD226
• PD1
• cancer immunotherapy
• virus
• antibodies

Disclosure of Potential Conflicts of Interest

All authors are employed by Genentech, Inc., a for profit company.