Janus Kinase Inhibitor as novel treatment of atopic dermatitis: A review

Known as a multifactorial illness, atopic dermatitis (AD) affects up to 20% of children and 10% of adults and is characterized by chronic inflammatory skin conditions. However, the whole pathophysiology of AD has not yet been completely understood. Janus kinase (JAK) inhibitors have recently become a novel therapeutic approach for the treatment of AD. The STAT (signal transducer and activator of transcription) transcription factor is phosphorylated after the transphosphorylation of the JAK receptor, which activates the JAK receptor. Following dimerization, STAT moves into the cell nucleus to alter gene transcription. Inhibition of JAK receptors prevents their transphosphorylation, which in turn prevents STAT's phosphorylation and dimerization, eventually prevents the production of inflammatory cytokines and dampens the inflammatory response as a whole. Differing JAK inhibitors with various isotype specificities have been created recently. By focusing on JAK signaling molecules downstream, JAK inhibitors in the context of AD can target a number of pruritogenic pathways. Consequently, oral and topical JAK inhibitors are viewed as novel AD treatments, particularly for individuals with persistent pruritus. In conclusion, JAK inhibitor are a potential new therapy option for AD and have been shown in several trials to be successful in symptom relief, improving quality of life, and enhancing psychological well-being of patients. Despite the encouraging results, further research is required to gauge the effectiveness and safety of JAK inhibitors.