REGENERATIVE medicine—the idea that it is possible to revitalise old, dilapidated tissue and keep a body going when its organs start to fail—is attractive. Much effort has thus been put into creating and nurturing so-called pluripotent stem cells. These, when appropriately nudged, can be induced to turn into cells of any other type. They might therefore be used for all sorts of repairs. Pluripotent cells, which once had to be extracted from embryos, can now be made routinely from body cells (skin cells, for example). Experiments are going on to see if, when made from the cells of a particular individual, they might be used to repair damage to that person’s organs without (as a transplant from someone else would) attracting the attention of his immune system.

This approach is promising. It would be even better, though, if rather than having stem cells transplanted into it, a degenerate organ could be persuaded to repair itself. Until now, no one has managed to do this. But Clare Blackburn of Edinburgh University in Britain, and her colleagues, have succeeded. As they report in Development, they have treated, in mice, an organ called the thymus, a part of the immune system that runs down in old age. Instead of adding stem cells they have stimulated their animals’ thymuses to make more of a protein known as FOXN1. This is a transcription factor (a molecular switch that activates genes), and for the thymus it turns out to be an elixir of life.

The thymus is the place where the immune system’s T-cells mature. T-cells have various jobs, such as destroying body cells infected with viruses. As an animal grows older, its thymus shrinks and the organ’s internal structure changes. As a result, the supply of new T-cells diminishes. That is why elderly people are more subject than the young to infection.

Dr Blackburn knew from earlier experiments that FOXN1 is important for the embryonic development of the thymus, so she wondered if it might be used to rejuvenate the organ in older animals. To this end, she and her colleagues bred a special strain of mice whose FOXN1 production could be stimulated specifically in the thymus by tamoxifen, a drug more familiar as a treatment for breast cancer.

Wild mice are normally killed by predators before they are a year old, but cosseted domestic versions often make it to two or even three, so Dr Blackburn and her team did their experiments on year-old and two-year-old animals, as being roughly equivalent to middle-aged and elderly humans. In year-olds, stimulating FOXN1 production in the thymus caused it to become 2.7 times bigger within a month. In two-year-olds the increase was 2.6 times. Moreover, when the researchers studied the enlarged thymuses microscopically, and compared them with those from untreated control animals of the same ages, they found that the organs’ internal structures had reverted to their youthful nature. Most important of all, they found, the density of relevant T-cells in the experimental animals’ lymph was twice that of the controls.

This is not a model for a medical treatment. Dr Blackburn relied on specially bred mice for the study. FOXN1 is not naturally sensitive to tamoxifen. But this work does provide an opening for regenerative medicine to exploit because it shows that, in the case of the thymus, stimulating production of a single transcription factor can have an astonishing effect—bigger, certainly, than anything yet seen using stem cells. Whether something similar applies to any other organ remains to be investigated. But Dr Blackburn’s study suggests it might be worth looking.