In the human immune system, T cells are important "soldiers" to defend health. When T cells recognize cancer cells, they attack. However, some cancer cells will bring a "mask" to themselves, avoiding the "scanning system" of T cells. PD-L1 protein is one of the important "masks" of cancer cells. At the same time, it also found an "alliance" - PD-1 protein on T cells. Once the two are combined, T cells cannot recognize and attack cancer cells.

Based on this finding, scientists have thought that if the interaction between PD-1/PD-L1 is disrupted, it will enable T cells to regain their anticancer effects. The success of the PD-1/PD-L1 antibody demonstrates this conjecture. Unfortunately, such antibodies do not "awake" all patients' T cells. Researchers have also been looking for the reasons behind and the ways to overcome them.

A Science: Finding Cancer Immunotherapy "Fuel"

Recently, a team of scientists from Emory University published an important achievement in the journal Science entitled "Rescue of exhausted CD8 T cells by PD-1–targeted therapies is CD28-dependent". The study found that even though the PD-1 brake was "destroyed", tumor-specific T cells still needed other "fuels" to expand their team and repair an effective immune response. This "fuel" comes from a co-stimulation of a molecule called CD28.

Professor Rafi Ahmed, author of the study and director of the Emory Vaccine Center, said: "This study suggests that the presence of CD28 on T cells may be a clinical biomarker for predicting whether a drug targeting PD-1 will be effective. The demand for CD28 suggests that some patients may be missing this co-stimulation, which will help guide the design of the combination therapy."

Professor Rafi Ahmed, a world-renowned immunologist and member of the American Academy of Sciences

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