In a new study, researchers reveal an important player that promotes skin inflammation in atopic dermatitis and the characteristic thickening of the skin. Severe eczema, also known as atopic dermatitis, is a chronic inflammatory skin condition that is driven by an allergic reaction. The study published in the Journal of Experimental Medicine.

A member of the tumor necrosis factor (TNF) super family, directly controls the hyperproliferation of keratinocytes as well as the expression of periostin, a protein that contributes to the clinical features of atopic dermatitis as well as other inflammatory skin diseases such as scleroderma.

"Periostin is being used in the clinic as a marker for allergic diseases such as asthma as well as atopic dermatitis," explains senior author Michael Croft, Ph.D., professor and head in the Division of Immune Regulation. "The fact that LIGHT acts upstream of periostin and is controlling its production really reinforces the idea that this is potentially a very good clinical target for treatment of atopic dermatitis and other inflammatory skin diseases."

In fact, a therapeutic antibody that neutralizes the activity of LIGHT successfully suppressed disease symptoms after they first appeared, suggesting that therapies based on blocking LIGHT may add a valuable treatment option for patients suffering from severe eczema, an often debilitating disease.

In an earlier study,they had shown that LIGHT plays a key role in skin inflammation in scleroderma, an autoimmune disease that results in the overproduction of collagen leading to the thickening and scarring of tissue. But whether LIGHT signaling is also involved in other types of skin inflammation was unknown.

A closer look revealed that LIGHT stimulates the proliferation of keratinoyctes and thus the structural remodeling of the skin. It also showed that LIGHT strongly induces the expression of periostin. This protein is highly expressed in the skin of patients with atopic dermatitis and scleroderma, and animal studies have found it is essential for skin inflammation, although exactly how it functions is still being debated.

The researchers then went back and used an existing therapeutic antibody to block the interaction of LIGHT with its receptor, HVEM, after disease had already manifested. Author concludes that  therapies that block LIGHT signaling might halt atopic dermatitis in humans and maybe even reverse disease symptoms.