If memory T cells are re-stimulated properly, they can kill the cancerous cells before PTLD develops, VanBuskirk says. But if that re-stimulation is weak or is blocked, not all of the cells are destroyed and cancer can develop. So it is critical that these two cell types work together effectively.
The present study suggests that PTLD arises because the scout cells can only weakly activate the memory T cells and stop their activation by other cells.
VanBuskirk and her team believe this happens because an immune-system substance causes changes in the scout cells, inhibiting their ability to warn memory T cells about the virus. That substance is called transforming growth factor-beta (TGFb).
The researchers discovered this by exposing healthy human scout cells to TGFb. Next, they combined the scout cells with T cells and PTLD-like cancer cells.
The T cells that grew alongside the scout cells exposed to TGFb were significantly less able to kill the cancer cells than were the T cells growing with scout cells not exposed to TGFb.
In addition, when scout cells from both groups were combined, the TGFb-exposed cells were stronger and prevented the unexposed scout cells from re-stimulating the memory T cells.
The present study follows earlier research led by VanBuskirk that suggests why only some transplant patients develop PTLD and not others.
The earlier study, published in a February 2005 issue of the journal Blood, suggested that the balance in the body of TGFb and a second immune substance called interferon gamma (IFNg) might influence development of the cancer.
The study showed that so
Source:Ohio State University