Anti-CTLA-4 checkpoint inhibition is thought to work by decreasing regulatory T cells’ (Tregs) ability to suppress anti-tumor responses. However, Tregs also help limit inflammation, so anti-CTLA-4 treatment is often associated with adverse inflammatory effects. Therefore, Dr. Pedros is investigating how a Treg enzyme and a CTLA-4-associated protein complex promote Tregs’ ability to suppress anti-cancer immune responses. When that enzyme was disabled, it prevented Tregs’ pro-cancer activity and eliminated tumors in mice. Importantly, this didn’t affect Tregs’ ability to prevent inflammatory colitis, a dangerous side effect seen in some patients treated with anti-CTLA-4 antibodies. Dr. Pedros’ next step is to further define how this enzyme regulates the pro-cancer function of Tregs. His work may result in new approaches to target this enzyme and suggest promising ways to promote anti-cancer immune responses with fewer side effects in Treg-based human therapies.
I want to better understand the specific mechanisms that prevent the immune system from efficiently eliminating cancer cells and to identify and validate some novel, clinically relevant immunotherapeutic targets. Obtaining financial support gave me some peace of mind and allows me to stay focused on scientific matters only.
Projects and Grants
Control of regulatory T cell function by protein kinase C-eta (PKCη): A novel target for cancer immunotherapy
La Jolla Institute for Immunology | All Cancers, Melanoma, Prostate Cancer | 2016 | Amon Altman, Ph.D.
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