Drugs Targeting Type 2 Inflammation May Aid Skin Barrier Function in Atopic Dermatitis

Systemic treatments that target type 2 inflammatory pathways may improve skin barrier dysfunction in atopic dermatitis, according to a review published in JID Innovations.

“Skin barrier dysfunction in atopic dermatitis is driven by genetic predisposition, environmental factors, and inflammation,” explained lead and corresponding author Lisa A Beck, MD, of the University of Rochester Medical Center, Rochester, New York, and coauthors.

While detergents, pollutants, food emulsifiers, and other substances in modern environments are thought to contribute to atopic dermatitis and other allergic diseases, type 2 inflammatory cytokines have been shown to play a key role.

“Targeting type 2 cytokines in atopic dermatitis has a broad range of beneficial effects on the components of the skin barrier,” the paper states, “including lipids, proteins, skin pH, corneocyte structure, tight junctions, sweat glands, and the microbiome, reinforcing the notion that atopic dermatitis is a systemic type 2 inflammatory disease.”

The article reviews evidence on the effects of specific treatments developed to target type 2 inflammatory pathways, including the oral Janus kinase inhibitors gusacitinib and tofacitinib, as well as the monoclonal antibodies dupilumab and tralokinumab—and investigational fezakinumab and GBR830. Despite available data on their effects on the skin barrier, there is more to be learned, the authors noted.

“Further research is needed to confirm to what extent type 2 targeted therapies can improve skin barrier function,” they advised, “and what role this barrier repair plays in the clinical improvement seen in atopic dermatitis.”

Reference:
Beck LA, Cork MJ, Amagai M, et al. Type 2 inflammation contributes to skin barrier dysfunction in atopic dermatitis. JID Innov. Published online April 26, 2022. doi:10.1016/j.xjidi.2022.100131