Research round-up: autoimmune disease
Tissues' shared response to attack
Type 1 diabetes, lupus, multiple sclerosis and rheumatoid arthritis can all be characterized as the immune system attacking a person’s own tissues. There are also commonalities in the way this attack is launched, with several shared mediators of tissue damage. The tissues affected in each disease are different. But researchers led by Decio Eizirik at the Indiana Biosciences Research Institute in Indianapolis have shown that how these tissues respond to immune assault in each disease is remarkably similar — although the target cells vary considerably, the path to destruction is shared.
The team used gene-expression data sets from each of the affected tissues — the pancreas, kidneys, optic chiasm and joints — and looked for similarities and differences during the inflammatory response in people with and without disease. They found changes in the expression of major common sets of genes in the target tissues of all four diseases. One of the shared molecular signatures is the gene that codes for TYK2, a protein involved in the regulation of a key immune modulator, interferon.
The activation of common molecular signatures suggests drugs already in use to treat one autoimmune disease could be equally beneficial for another. In separate studies, it has been found that TYK2 inhibitors have a protective effect against immune-mediated damage in psoriasis and type 1 diabetes. The authors say that their work demonstrates the benefit of focusing not only on the immune attack, but also on how the target tissues respond to immune cells.
To read the full article, go to Nature Outlook.