Abstract
Autoimmune skin diseases are characterized by significant local and systemic inflammation that is largely mediated by the Janus kinase (JAK)–signal transducer and activator of transcription (STAT) pathway. Advanced understanding of this pathway has led to the development of targeted inhibitors of Janus kinases (JAKinibs). As a class, JAK inhibitors effectively treat a multitude of hematologic and inflammatory diseases. Growing evidence suggests that JAK inhibitors are efficacious in atopic dermatitis, alopecia areata, psoriasis, and vitiligo. Additional evidence suggests that JAK inhibition might be broadly useful in dermatology, with early reports of efficacy in several other conditions. JAK inhibitors can be administered orally or used topically and represent a promising new class of medications. Here we review the evolving data on the role of the JAK-STAT pathway in inflammatory dermatoses and the potential therapeutic benefit of JAK-STAT antagonism.
Highlights
Reviewed by: Massimo Gadina, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), United States Kunihiro Yamaoka, Keio University School of Medicine, Japan
The results show that significantly more patients treated with ruxolitinib cream for 24 weeks achieved a ≥50% percent improvement from baseline in the facial Vitiligo Area Scoring Index (VASI) score compared with patients treated with a control vehicle [(66); World Congress of Dermatology; June 2019; Milan, Italy]
Despite phenotypic differences in the inflammatory mediators responsible for driving disease pathogenesis, these aforementioned dermatoses are characterized by increased inflammatory mediators that signal through the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway
Summary
Autoimmune skin diseases are characterized by significant local and systemic inflammation that is largely mediated by the Janus kinase (JAK)–signal transducer and activator of transcription (STAT) pathway. Advanced understanding of this pathway has led to the development of targeted inhibitors of Janus kinases (JAKinibs). Upon binding of ligand to its cognate cytokine receptor, associated JAKs become activated and undergo autophosphorylation and transphosphorylate the intracellular tail of their receptors This creates docking sites for the SH2 domain of the cytoplasmic transcription factors termed signal transducers and activators of transcription (STATs). IL-6 produced by activated dendritic cells (DCs) is a key factor in promoting Th17 differentiation via STAT3 and retinoic acid receptor–related orphan receptor γ (RORγt) induction [7] with IL-23 critical for memory Th17 in vivo function [3, 8]
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