Re-education of macrophages
Scientists have "reprogrammed" innate immunity to fight pancreatic cancer
Researchers from Rush University Medical Center (USA) have developed a molecule that binds to macrophages "deceived" cancer cells, which force it not to attack the tumor. The molecule "reprograms" macrophages and reminds them of their main mission – to attack pancreatic cancer cells, according to a press release Immune-boosting compound makes immunotherapy effective against pancreatic cancer. The results of the study are published in the journal Science Translational Medicine (Panni et al., Agonism of CD11b reprograms innate immunity to sensitize pancreatic cancer to immunotherapies – VM).
Macrophages (translated from Greek as "big eaters") are cells in the body of animals and humans that can capture and digest bacteria, the remains of dead cells and other foreign or toxic particles for the body. In a good way, they should also kill cancer cells. But malignant tumors affect the tissues that surround them, including the macrophages contained in the tissues. Cancer tricks these cells and turns them into accomplices - macrophages associated with the tumor – that do not attack the harmful cells. And in pancreatic cancer tumors themselves, the number of macrophages that help tumors grow far exceeds the number of those that suppress them.
Macrophages can be "reprogrammed," as a new study shows. A specially developed molecule ADH-503, which activates the CD11b protein found on the surface of macrophages, will help in this. It is a receptor protein that detects threats and transmits signals about whether the immune system should respond.
ADH-503 binds to the CD11b protein and on the surface of macrophages and activates it. When the researchers orally delivered the ADH-503 compound to mice with pancreatic cancer, the number of macrophages in and near the tumors decreased, and the remaining macrophages were shown to stimulate, rather than suppress, immune responses. This environment led to more cancer-destroying T cells in the tumor, significantly slowing the growth of the tumor.
The researchers then tested how susceptible the pancreatic tumor environment was to standard immunotherapy. First, they treated a control group of mice with immunotherapy – a checkpoint inhibitor (PD-1 inhibitor), which is used to treat other cancers. There was no measurable effect. But when the therapy was combined with the ADH-503 compound, the tumors shrank and the mice lived significantly longer.
The authors of the development hope that their new compound will help to obtain new drugs for immunotherapy of pancreatic cancer.
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