Researchers at King’s College London have identified a new gene (PIM1), which could be an effective target for innovative treatments and therapies for the human autoimmune disease, psoriasis.
Psoriasis affects around 2 per cent of people in the UK and causes dry, red lesions on the skin which can become sore or itchy and can have significant impact on the sufferer’s quality of life.
It is thought that psoriasis is caused by a problem with the body’s immune system in which new skin cells are created too rapidly, causing a build up of flaky patches on the skin’s surface. It is not known exactly why this problem occurs but it is thought that certain genes may play a role.
The study, published today in Science Translational Medicine highlights for the first time the role of PIM1 and the IL-22 cytokine – a protein that sends messages between cells – in skin inflammation such as that seen in psoriasis patients.
Scientists, led by Professor Frank Nestle from the St John’s Institute of Dermatology at Guy’s and St Thomas’ NHS Foundation Trust and King’s College London, injected IL-22 into models of normal human skin in mice.
The changes that subsequently occurred in the skin were reminiscent of psoriasis. Injecting an antibody to block the IL-22 cytokine caused these changes to reverse.
They were then able to perform computer analysis, comparing the data from these human skin models with existing gene datasets, in order to identify the gene PIM1 as one of the genes ‘switched on’ by the presence of IL-22. They further showed that a small molecule drug blocking PIM1 was effective in models of psoriasis. The link between the IL-22 cytokine, which causes inflammation, and subsequent changes in the PIM1 gene suggests a direct link between PIM1 and psoriasis.