Immunotherapy has emerged as a key weapon in the fight against cancer. However, nearly 80% of patients either don’t respond to these treatments or they become unresponsive after initially responding to the immunotherapy. The scientific community has been grappling with how to improve response rates, and a new study uncovering how cancer cells reprogram our immune cells to support cancer growth could provide a key.
The study, whose findings were published in Science Immunology, was conducted by a team at the University of Texas at Dallas. The team found that cancer doesn’t just hide from immune cells. Rather, it actively reprograms the immune cells within the tumor microenvironment so that they become suppressed and cannot mount an attack against the tumor.
The scientists found that a protein on the cancer cells hijacks parts of the immune system called myeloid cells by binding to them and reprogramming the immune cells so that they become allies of the malignancy. When this reprogramming happens, it becomes futile to treat the patient using a checkpoint inhibitor.
The problematic cancer proteins are called claudins. They form tight bonds with myeloid cells and leverage a signaling pathway through which inflammation and the protective attributes of the immune system are regulated.
The researchers leveraged mouse models and data on cancer in humans to make this discovery. They found that the myeloid cells tended to exist in the same microenvironment as claudins, and the interaction between these components impacted the rate at which cancer thrived. With myeloid cells compromised by claudins, there was an acceleration in the rate at which tumors grew.
In contrast, healthy human tissues had minimal claudin interaction with myeloid immune cells, and cancer couldn’t grow in such an environment.
The researchers explain that their findings have significant implications for immunotherapy. They say that existing immunotherapies could become more lethal against cancer even in patients who had become unresponsive if interventions are taken to disrupt claudin interaction with their immune system.
The study authors also say that testing for interactions between claudins and myeloid cells could help in identifying patients who are unlikely to respond to immune checkpoint inhibitor treatments and when such patients are identified, measures can be taken to disrupt the process through which cancer cell proteins bind to immune cells in order to suppress them. Once that happens, the checkpoint inhibitors can activate the immune system to attack the cancer.
This research offers a new way to understand why response rates to immunotherapy have been low and opens the door to unlocking the potential of these treatments for a lot more patients.
It would be interesting to hear what companies like CNS Pharmaceuticals Inc. (NASDAQ: CNSP) think about these new revelations about how cancer disarms the immune system by turning immune cells into allies.
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