Keloid lesions exhibit increased IL-4/IL-13 signaling and respond to Th2-targeting dupilumab therapy, Mount Sinai researchers report.
Researchers, led by Emma Guttman-Yassky, MD, PhD, Vice Chair, Department of Dermatology at the Icahn School of Medicine at Mount Sinai in New York, presented a case study of a patient with moderate to severe atopic dermatitis (AD) who also had two keloids: one large and one small.
The patient was treated for AD with dupilimab and approximately 7 months later, one of the smaller keloids completely disappeared, with approximately 50 percent reduction in the size of larger keloid. Further investigations of lesional keloid and non-lesional skin from additional keloid patients identified high expression of IL-4R, Il-13 and an important mediator of type 2 pathway, CCL18.
The immune markers in the skin of keloid patients were increased not only in lesional skin but also in their non-lesional skin, which suggests that the entire skin layer of patients with severe keloids is abnormal and prone to additional keloid formation, supporting the use of systemic treatments.
“This major discovery is the first report to show a successful keloid response to the drug dupilumab, which blocks type 2- driven inflammation via IL-4/I-13 receptors,” Dr. Guttman-Yassky says in a news release. “The study also showed a disappearance of not only a small keloid but shrinkage of a huge keloid by 50 percent and therefore stands the chance to revolutionize the treatment of keloids.”
The new findings appear in the Journal of European Academy of Dermatology and Venereology.