A new form of cancer immunotherapy has shown good results in a trial run by scientists at University College London, UK, it has been announced.
The experimental drug targets regulatory immune cells inside a tumour, delivering a “two-pronged response”, say the scientists, led by Professor Sergio Quezada.
Their study, published in Nature Cancer on Monday (9 November), indicates that the drug significantly improves long-term survival in tests on mice.
The drug targets the CD25 protein on the surface of regulatory T cells, which are found at higher rates in cancerous tumours. Previous attempts to destroy regulatory T cells, and allow the immune system to attack the tumour, have not proved highly effective.
However, this new anti-CD25 drug appears to be more successful against CD25, as well as avoiding another drawback of previous drugs – it does not destroy the beneficial ‘effector’ T cells in the tumour. It will soon be tested in safety trials of patients with several types of cancer.
Professor Quezada says: “For many years it’s been a complex mystery, why targeting CD25 with other drugs has not been as effective as anticipated. Now, by going back to basic biology and unpicking the mechanism behind this protein we have found that targeting CD25 was absolutely the right approach, but we needed to target a different part of the protein.”
The study was partly funded by Cancer Research UK. Professor Karen Vousden, of the charity, commented: "Therapies that activate an immune response against cancers have already been a game changer for many tumour types, but they only work for a minority of patients.
“One approach to try to make them more effective has been to try to target immune cells called regulatory T cells, which normally limit the immune response.
“In this study, scientists have invented a new antibody that produces potent anti-tumour responses."
Solomon, I. et al. CD25-Treg-depleting antibodies preserving IL-2 signaling on effector T cells enhance effector activation and antitumor immunity. Nature Cancer 9 November 202 doi: 10.1038/s43018-020-00133-0
Leave a Reply