Your immune system is always busy fighting incoming threats. It consists of a system of cells, and when there is a shortage of cells, it affects the performance of the immune system. This is seen, for example, in cancer patients following chemotherapy. This is because chemotherapy targets all the cells in your body, including the stem cells in your bone marrow, which were meant to develop into new immune cells. This means that the immune system then lacks cells to fight new infections.

There are drugs that can harvest stem cells from the bone marrow, so that they can be returned to the patients after treatment. They then develop into new immune cells, enabling the body to once again fight incoming threats. But previously, we lacked detailed knowledge of how these drugs worked.

Now, a study conducted in mice by researchers at the University of Copenhagen demonstrates how the medicine works at the cell level—and, surprisingly, how one of the two applied and tested drugs is more effective than the other, despite the fact that the other drug, on paper, appears to be the most effective of the two. This discovery may not just help improve stem cell transplantation; it may also lead to improved drugs in the future. We have tested two drugs for stem cell transplantation which appear to have the same effect. What they do is block a receptor, causing the bone marrow to release stem cells into the blood. What the new study shows, though, is that they do not just block the receptor; one of the two drugs also affects other signalling pathways in the cell. And in short, that makes it more effective than the other of the two drugs.

Regards

John
Editorial Assistant
Immunogenetics Open Access