There is great potential in the destruction and recreation of the immune system: the removal of all immune cells and replacement with new cells. This is an approach capable of curing autoimmune conditions, but perhaps more importantly it might also be used to clear out much of the dysfunction of the aged immune system. Immune system decline is an important component of the frailty of aging, and it speeds other aspects of the aging process through inflammation and a growing failure to monitor and destroy potentially harmful cells, such as those that become senescent. Just recently researchers made real progress on the immune system destruction front, finding a way to achieve that goal without harmful chemotherapy, and to match that advance, here is news of a potential method to improve the restoration phase of the process:
New research has shown how a cell surface molecule, Lymphotoxin β receptor, controls entry of T-cells into the thymus; and as such presents an opportunity to understanding why cancer patients who undergo bone-marrow transplant are slow to recover their immune system. The thymus, which sits in front of the heart and behind the sternum, imports T-cell precursors from the bone marrow and supports their development into mature T-cells that fight off dangerous diseases. T-cells are often the last cells to recover in cancer patients receiving bone marrow transplants. Though the cancer is cured, patients are often left with an impaired immune system that can take years to recover. Researchers found that Lymphotoxin β receptor was required to allow the entry of T-cell progenitors to the thymus both in a healthy state, and during immune recovery following bone-marrow transplantation.
Significantly, the team also found that antibody-mediated stimulation of Lymphotoxin β receptor in mouse models enhanced initial thymus recovery and boosted the number of transplant derived T-cells. "Post-transplantation, T-cell progenitors derived from the bone marrow transplant can struggle to enter the thymus, as if the doorway to the thymus is closed. Identifying molecular regulators that can 'prop open' the door and allow these cells to enter and mature, could well be a means to help reboot the immune system. This is just one piece of the puzzle. It may be that there are adverse effects to opening the door to the thymus, but identifying a pathway that regulates this process is a significant step." Following these positive findings the team aim to move towards in-vitro samples of human thymus to examine the role that Lymphotoxin b receptor might play in regulation of thymus function in humans.