New findings suggest that eosinophilic cellulitis (EC) preferentially activates the Janus kinase (JAK) 1/JAK2-STAT5 pathways. The researchers behind the findings say this discovery warrants exploring JAK inhibitors as treatments for this condition.
The research was published online ahead of print in JAMA Dermatology (June 21, 2023).
“The pathogenesis of eosinophilic cellulitis is poorly understood, limiting available treatment options,” the authors write about the motivation behind this study. “The current treatment paradigm focuses on delayed type 2 hypersensitivity reaction to various triggers.”
This case series was conducted in Lyon, France, from Jan. 2018 to Dec. 2021. Researchers analyzed archival skin biopsy samples from 14 patients with EC and eight healthy control participants using histology, Janus kinase (JAK)–signal transducer and activator of transcription (STAT) immunohistochemistry, and gene profiling.
The investigators observed marked type 2 inflammation, indicated by the chemokines CCL17, CCL18, CCL26, and interleukin (IL)-13. They found preferential activation of the JAK1/JAK2-STAT5 pathways in EC lesions.
One patient with refractory EC experienced complete clinical remission of skin lesions after one month of treatment with the JAK1/JAK2 inhibitor baricitinib.
“These findings suggest that eosinophilic cellulitis is a type 2 inflammatory disease with preferential activation of the JAK1/JAK2-STAT5 pathways,” the authors write. “Together with the clinical response to baricitinib, our data advocate for the development of JAK1/JAK2 targeting treatment approaches in eosinophilic cellulitis and other eosinophilic diseases.”