Eczema treatments are expensive and carry some itchy side effects. But, in a recent study, researchers have identified skin cells as a natural barrier to the allergic attacks caused by the disease.
Today, about 17% of children in developed countries have eczema, an inflammation of the skin that causes redness and itching. Often, eczema is the gateway to other issues such as food allergy or asthma. There are treatments, like steroid creams, to reduce inflammation, but they are expensive, and often have side effects on the bones, the liver or the skin.
However, a study, published in the journal Science Immunology, suggests a different approach to treating eczema. A number of skin cells would be a natural barrier to the allergies caused by the disease.
“Regulatory” T cells slow down immune activity
The cutaneous inflammation of eczema is caused by a type 2 immune activity. However, a group of T cells, known as regulatory T cells — also commonly referred to as Tregs — have the ability temper the type 2 immune response. Regulatory T cells account for up to 50% of T cells in the skin, but in the rest of the body they account for only 5%.
The presence of a necessary protein
Researchers have discovered the importance of a protein called Retinoid Receptor (ROR). Indeed, by removing this protein in mice with eczema, they found that the Tregs stopped their activity. The influx of inflammatory cells has been multiplied by three. The allergy has developed. According to the scientists’ analysis, this is because without ROR, the cells make less TL1A, a receptor that activates the Tregs, but also the cells responsible for the inflammation. Tregs do not “see” TL1A in too small numbers, so there are more “inflammatory” cells that activate.
Several therapeutic approaches
With these discoveries, researchers see several lines of treatment. The first is to boost the level or activity of the retinoid receptors, through a cream for example. Another is to find factors in the skin that can stimulate the level of retinoid receptors themselves.