Although there’s currently no cure for the skin disease psoriasis, a new study has popped up that may give those living with the affliction some relief.
A recent study conducted at the Karolinska Institutet and published in the Journal of Allergy and Clinical Immunology proposes that the miR-146a gene can be a “chronicity factor” that helps the resolution of inflammation and may deter the disease from being persistent.
In Brief: What Is Psoriasis?
Similar to eczema, psoriasis is a common skin disease that presents itself as reddened, scaly patches of inflamed skin that can sometimes cover large parts of the body.
The development of the disease (also known as pathogenesis) is a combination of inherited and environmental factors. There is no known cure to permanently neutralize the affliction; patients are limited to remedies that soothe and reduce the symptoms.
The researchers at the Karolinska Institutet have already determined that microRNA (a cellular RNA fragment that prevents the production of a particular protein) named miR-146a exists in skin cells and protects against psoriasis. To determine its relation to the skin disease, they used a group of mice lacking miR-146a and a control group given miR-146a. By forcing psoriasis-like skin changes with a cream, they were able to measure the results in their lab.
The study shows that the gene miR-146a is a particular gene that protects against psoriasis. It acts as an anti-inflammatory in the skin, and adjusts the response of skin cells to IL-17, a cytokine—a substance secreted by certain cells of the immune system that has an impact on other cells.
The suppression of cytokine is one of the most powerful treatment interventions for the disease. To sum it all up, the study found that the injection of synthetic miR-146a had a noticeable effect on the mouse model by effectively relieving the inflammation.
Sirvastava et al., “MicroRNA-146a suppresses IL-17 mediated skin inflammation and is genetically associated with psoriasis,” JACI Online web site, August 24, 2016; http://dx.doi.org/10.1016/j.jaci.2016.07.025