Autoimmune conditions such as rheumatoid arthritis result from errant cellular behavior in the immune system - immune cells are instructed to attack healthy tissue rather than performing beneficial tasks such as hunting down cancerous or senescent cells. As researchers become better at controlling cellular behavior, reprogramming cells for desired tasks by sending the right chemical signals, this type of disease will become a treatable nuisance rather than a life-destroying condition. Here is an example of the sort of work presently taking place:
Normally, immune cells develop to recognise foreign material - antigens; including bacteria - so that they can activate a response against them. Immune cells that would respond to 'self' and therefore attack the body's own cells are usually destroyed during development. If any persist, they are held in check by special regulatory cells that provide a sort of autoimmune checkpoint. A key player in these regulatory cells is a molecule called Foxp3.
Dr. Alexander Betz, Group Leader at the MRC laboratory, explains: "We have generated a modified form of Foxp3 which can be introduced into immune cells using genetic engineering techniques and then activated by a simple injection. When administered to and activated in animal models of arthritis, the modified cells inhibit or even reverse the disease process."
Further work is now aimed at elucidating the detailed molecular mechanisms involved in Foxp3 function, and transferring the experimental approach to human cells.
It's a road of a decade or more in the present over-regulated environment to move from a promising therapy in mice to human therapy in late clinical trials. But many groups are working on the reprogramming of immune cells: it is a broad field of endeavor, and advances in the state of the art made by any one group benefit all the others.