Eczema, also known as atopic dermatitis, is a very common chronic skin disease. Eczema often begins to appear in early childhood, although called “wet” rash, it can make the original delicate skin become dry, swollen and thickened, and may also bring persistent strong itching, which makes people very uncomfortable. Some children’s symptoms will subside with age, but many children’s symptoms will continue to teenagers and adults. < / P > < p > in a recent study led by Cincinnati Children’s Hospital Medical Center, scientists have found a new genetic factor in the pathogenesis of eczema. They found two common variants of a gene called KIF3A, which can cause skin barrier damage, cause skin dehydration, promote eczema, and increase the risk of diseases such as asthma and food allergy. < / P > < p > under normal conditions, KIF3A protein is an essential part of cell ciliary structure. This cilia acts as an antenna on the cell surface, helping to receive important sensory signals from other cells. < / P > < p > however, the researchers found that there are two common single nucleotide polymorphism (SNP) genetic variants in KIF3A. Although it is only a small change of single nucleotide in DNA sequence, they will reduce the production rate of KIF3A protein by changing the degree of gene methylation. In skin cells and nasal mucosa cells, the amount of KIF3A protein produced by the two variants decreased by nearly 20% compared with that of normal KIF3A. The relationship between the low expression of KIF3A and the damage of skin barrier was verified by further animal experiments. When the researchers deprived mice of KIF3A in their epidermal cells, they found that as the adhesion of epidermal cells decreased, their skin became more prone to water loss. Measuring the rate of such skin loss is also a way to determine the severity of eczema in children, the researchers said. In addition, skin inflammation, swelling and thickening similar to eczema were observed in these mice with skin deficiency of KIF3A. This means that when the skin barrier is damaged and the skin is drier, it is also easy for allergic substances in the environment (such as pollen, dust mites, etc.) to penetrate into the skin, increasing the possibility of eczema. It is worth mentioning that the dysfunction of KIF3A gene is related to other common allergic diseases. In previous work, the researchers found that dysfunction of KIF3A in lung tissue can lead to asthma; in intestinal tissue, dysfunction of this gene may increase the risk of food allergy. < / P > < p > the researchers thus pointed out that the new findings can link the two kinds of allergic risks with the damage of skin barrier, which means that more allergenic substances enter our bodies, leading to the over reaction of the immune system. “We are trying to uncover the link between skin, gut and lung health.” Said Dr. gurjit Khurana Hershey, who led the study. < / P > < p > in addition to understanding the mechanism of these common diseases, this discovery will help to bring new rapid screening methods. Not long ago, the team developed a test method for collecting skin cells from young children with painless tape. Hershey said they plan to use cell samples collected with tape to quantify patients’ KIF3A expression to predict the risk of eczema. < / P > < p > more importantly, this information will help people with genetic risk to actively take intervention measures, such as enhancing local moisturizing and preventing skin moisture loss. Early prevention of eczema is likely to further help prevent asthma and other allergic diseases. < / P > < p > in addition, the team also said that they have begun to look for drug compounds, hoping to repair the KIF3A gene and solve a series of problems caused by skin barrier damage.