ENGINEERINGNET.BE – Detecting abnormal cells in the human body is normally a task of T cells, white blood cells that play an important role in the immune system. These cells can recognize many types of abnormalities, such as infections with viruses and bacteria.
But the immune system sometimes has trouble detecting cancer cells. These malignant cells are only recognized by T cells if a specific molecule is attached to them. To escape the immune system, some cancer cells lack this molecule, making them “invisible” to conventional T cells.
Researchers from the Leiden University Medical Center and the Netherlands Cancer Institute observed a strange phenomenon: some patients with ‘invisible’ tumors respond very well to immunotherapy against cancer.
In these therapies, in particular, the activity of T cells is stimulated or enhanced by antibodies. ‘But these cancers lack the molecules that enable T cells to recognize them. We therefore did not understand why the patients responded so well to the treatment,’ says Noël de Miranda, leader of the Cancer Immunogenomics research group at the LUMC.
Further investigation of cells from patients treated at the Antoni van Leeuwenhoek Hospital shows that so-called γδ T cells, a less well-known, specialized type of immune cell, are able to detect cancer cells that are invisible to conventional T cells.
De Miranda: ‘This shows that our immune system has a kind of back-up: a second line of defence. Our findings may eventually lead to new treatments of ‘invisible’ tumors with this type of T cells.’
“We are only just beginning to unlock the potential of γδ T cells for the development of new immune therapies for cancer,” says Emile Voest, professor of medical oncology, group leader at the Netherlands Cancer Institute/Antoni van Leeuwenhoek and researcher at Oncode.
‘We now have a better understanding of how these immune cells work against tumors in cancer patients and how we can use them to develop new immune therapies.’
The research is funded by Oncode and the European Research Council.