Bone marrow transplants can treat a variety of blood diseases including sickle cell anemia. The hematopoietic stem cells (HSCs) delivered in a transplant can generate all sorts of blood cells, and replace faulty patient cells with functioning ones. To avoid rejection of the transplanted cells, however, patients' own HSCs must be severely depleted with chemotherapy or radiation before the transplant, causing devastating side effects. These treatments can be omitted for patients with serious immune deficiencies, but even then transplants don't take well.

One explanation for this is that the transplanted HSCs can't attach into the proper place inside bones because the patient's faulty cells are already there. Publishing in Science, researchers led by Deepta Bhattacharya and Irving Weissman at Stanford University provide further evidence for this idea, and also show that, at least in mice, antibodies can be gentler than drugs at clearing the host's cells to make room for the transplanted ones.

The researchers dosed mice with an antibody that blocks the signals that stimulate HSCs to grow and divide. After testing several, they selected an antibodiy that sticks to c-kit, a surface protein found on HSCs. They treated mice with the antibody and found that most endogenous HSCs disappeared from bone marrow.

After waiting a week for the antibody to be cleared from the mice's systems, the researchers transplanted bone marrow cells. They saw very high levels of engraftment, and the HSCs produced functioning immune cells. However, as Weissman told ScienceNow it's unclear whether an antibody that works as well in humans can be identified. Also, since some of the host's HSCs remain, they could compete with donor HSCs or even attack them. However, the research does show, in principle, that less harsh treatments could be perfected.