Opinion
Video
Author(s):
Peter Lio, MD, and Lisa Swanson, MD, PhD, provide an overview of Janus Kinase (JAK) inhibitors, their pathophysiology, and their mechanism of action in the treatment of atopic dermatitis (AD).
This is a video synopsis/summary of a panel discussion involving Christopher Bunick, MD, PhD; Peter Lio, MD; Lisa Swanson, MD, PhD; and Alexandra Golant, MD.
In this segment, Peter Lio, MD, introduces Janus kinase (JAK) inhibitors and their significance in molecular signaling pathways, particularly in diseases like atopic dermatitis. Originally named "just another kinase," JAKs play a crucial role in cellular signaling, with subtypes such as JAK1, JAK2, JAK3, and TKY2 (tyrosine kinase 2) associated with various diseases. Dr Lio explains that when inflammatory cytokine messages are transmitted between cells, they activate JAKs through conformational changes in receptor proteins. This, in turn, activates statin, influencing gene transcription in the nucleus.
Reflecting on the past, the discussion shifts to the initial belief that the JAK-STAT pathway was not druggable. Lisa Swanson, MD, PhD, highlights the progress, especially in the treatment of atopic dermatitis. The mechanism of JAK inhibitors is explored, focusing on their ability to interrupt the inflammatory process driven by cytokines binding to cell receptors. By inhibiting JAKs, the cascade of inflammatory processes is disrupted, impacting various cytokines and their role in gene transcription.
The conversation emphasizes the evolving understanding of atopic dermatitis as a multi-cytokine disease, with JAK inhibitors providing insights into the heterogeneity of the condition. The inhibitors not only address inflammation but also contribute to a deeper comprehension of the role of different cytokines in both skin inflammation and itch. Overall, the discussion underscores the transformative impact of JAK inhibitors in the field of dermatologic treatment and research.
Video synopsis is AI-generated and reviewed by HCPLive editorial staff.