In a new study, mouse models of pancreatic cancer were treated with a RAS inhibitor plus an agent called 21h10, an AI-designed mimic of an immune-related cytokine called interleukin (IL)-21. The combination initiated an immune response that turned the transient effects of RAS inhibition into a durable response. The work is published in the journal Cell.
The team found that 21h10—which was designed by David Baker’s lab at the University of Washington to be more stable and have better drug-like qualities than naturally occurring IL-21—primes and activates CD4 T cells in the cancer. These T cells produce a signal called interferon-γ (IFN-γ), which induces innate immune cells called macrophages to destroy tumor cells.