A virtually unlimited supply of rare cells can now be produced in the laboratory to fight diseases such as rheumatoid arthritis in mice.

Crucially, these cells, which dampen down the body’s immune response, have been engineered so that they target damaged tissue yet don’t leave the rest of the body open to infection.

Vaccines have long harnessed the body’s natural ability to fight disease. Therapies that boost our natural immune response to cancer are also in the works (see Autoimmune disease cells harnessed to fight cancer).

But in autoimmune disease – in which the immune system mistakenly attacks the body’s own tissue – the opposite is needed. So immunologists have long eyed up the cells that dampen down the immune response, known as regulatory T-cells or T-regs, for their potential to treat autoimmune disorders such as rheumatoid arthritis, diabetes and multiple sclerosis.


There have been two challenges: how to obtain large supplies of the rare T-regs, which make up less than 1 per cent of all immune cells, and how to neutralise dangerous immune cells without weakening the entire immune system, leaving people open to infection. Now Hans Stauss and his colleagues at University College London have made a stab at solving both.

Straight to the joint

The team starts by extracting ordinary T-cells – immune cells that are common in the blood – from mice and using a virus to insert two genes into these cells. One gene, FOXP3, transforms the ordinary T-cells into T-regs. The second gene codes for a receptor for a substance called ovalbumin.

Next the researchers injected ovalbumin into mice with rheumatoid arthritis, which is caused by normal T-cells attacking cartilage. Each mouse had two arthritic joints, but the researchers injected the ovalbumin into one only. Then they injected the lab-produced T-reg cells into the same mice.

The idea was that the ovalbumin would attract the cells, which would dampen down the arthritic inflammation that was attacking the joint’s cartilage. The rest of the immune system, however, would remain intact.

Sure enough, the injected cells homed in on the ovalbumin-injected arthritic joints and reduced inflammation, while the other joints remained inflamed.

More targets

Stauss says that a similar T-reg therapy could be developed to target autoimmune diseases that strike other parts of the body, by adding genes for receptors specific to molecules found there.

Alexandre Corthay of the University of Oslo in Norway warns of the unpredictable nature of T-regs, which regularly turn back into normal T-cells in the body. Stauss admits that this is a risk but reckons that artificially produced T-reg cells are more stable than naturally occurring ones.

He also points out that because the T-regs are specific to a particular part of the body, even if they did revert, the damage they could do would be limited.

Journal reference: Proceedings of the National Academy of Sciences, DOI: 10.1073/pnas.0907396106