According to a story from Scleroderma News, the results of a recent mouse study could have significant implications for the future of scleroderma treatment. In the study, scientists used a modified version of a certain inflammatory protein to reverse fibrosis (scarring) that characterizes the illness. The original study can be found in the scientific journal Nature Communications.
About Scleroderma
Scleroderma, which is also referred to as systemic sclerosis, describes a group of autoimmune diseases that can cause system-wide effects in the most severe cases. The mechanism of this disease is believed to be an autoimmune response in which the immune system mistakenly attacks body tissue. Some factors that may contribute to triggering the autoimmune response include mutations of the HLA genes and exposure to certain materials, such as certain solvents, white spirits, ketones, and silica. Symptoms are broad ranging and systemic, including kidney failure, erectile dysfunction, fatigue, stroke, headaches, facial pain, congestive heart failure, skin abnormalities, high blood pressure, chest pain, indigestion, and many more. Treatments are varied and depend on the symptoms, but most patients take medications in an attempt to suppress the autoimmune response. In severe cases, life expectancy is around 11 years from onset. To learn more about scleroderma, click here.
The TRAIL Protein
The key component in this research is a certain protein called TRAIL (tumor necrosis factor-related apoptosis-inducing ligand). This is an inflammatory protein that has the capability to trigger death in certain cells (primarily cancer cells). This makes TRAIL look like a good treatment for cancer, but so far there hasn’t been much progress. Researchers developed a modified version of TRAIL called TLY012, which was effectively just a more stabilized version.
Prior research revealed that TRAIL can destroy the cells that cause liver fibrosis. These scarring cells are called myofibroblasts. Researchers then took a sample of these cells from five healthy people and five scleroderma patients. The researchers found that the TLY012 could kill the cells from patients, but spared the cells from the healthy volunteers. To follow up on this finding, the protein was tested in two different scleroderma mouse models.
The results were impressive, and TLY012 had considerable benefits in both models, reducing both scarring and the thickening of skin. While more research is necessary, it appears that this protein could be a useful treatment for scleroderma and other scarring diseases.
