Scientists have identified a common genetic defect underlying psoriasis, rheumatoid arthritis and systemic lupus erythematosus (SLE), all of which are autoimmune disorders. Three different genes, all of which are controlled by the same protein 'switch', called Runx1, appear to be involved. The findings, reported in the journal Nature Genetics last week, could help in the search for new treatments for these diseases.
The symptoms of autoimmune diseases appear when the body's immune system attacks its own tissues. In psoriasis, patches of itchy, scaly skin appear on the patient's body, whereas in SLE and rheumatoid arthritis, the blood cells and joints respectively are affected. Researchers at the Washington University School of Medicine in St Louis have found a genetic alteration in psoriasis patients that affects one of the 'docking sites' of Runx1, which is located in the control region of another gene. Runx1 is a transcription factor, which means it controls the activity of other genes by sticking to such docking sites and switching on the associated gene.
In 2002, a team from the University of Uppsala in Sweden reported that many SLE patients have an altered Runx1 docking site, in the control region of a different gene to the one implicated in psoriasis. And another study reported in Nature Genetics last week, by a team from the Institute of Physical and Chemical Research in Yokohama City, Japan, showed that a third Runx1-controlled gene is involved in rheumatoid arthritis. All three genes appear to make proteins involved in the 'programming' of the immune system to distinguish between body cells and foreign invaders. It seems that when not regulated properly, such genes can contribute to the onset of autoimmune disorders.
It is likely that several other genes, as well as environmental factors are involved in psoriasis, rheumatoid arthritis and SLE. 'We're just putting together the first pieces of a big puzzle' said Anne Bowcock of the Washington team.