New Targets for Atopic Dermatitis and Chronic Itch: Neuroimmune Biology, OX40, JAK Inhibitors, and What's Coming
Dermatologists, NPs, and PAs: This session cuts straight to the clinical questions that matter most in atopic dermatitis right now.
Shawn Kwatra, MD, chair of dermatology at the University of Maryland School of Medicine and director of its dedicated itch center, joins hosts Joseph Merola, MD, MMSc, FAAD, FACR, and Alice Gottlieb, MD, PhD, to break down the neuroimmune biology of chronic itch, why pruritus persists even after skin clears, and what to do about it in your next clinic.
Topics covered:
- Why chronic itch is a neuroimmune disorder—not just a downstream symptom of inflammation
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The cytokine players: IL-4, IL-13, IL-31, TSLP, and how they directly sensitize sensory neurons
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Disease control redefined: the International Eczema Council consensus statement on low disease activity and remission in atopic dermatitis (published in JAMA Dermatology)
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What to do when skin clears but itch doesn't—JAK inhibitors, IL-31 inhibition, and neuromodulators
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Bispecific and trispecific approaches: why AD's biologic redundancy may require layered targeting
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OX40 and OX40 ligand: the upstream "prequel to inflammation" and its potential for off-therapy remission
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Phenotype-driven treatment: TH17/TH22 involvement, skin of color presentations, and where the field is heading
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Device-based modalities: phototherapy, TENS units, cold plasma—what the evidence actually supports
Want CME credit? Attend the next Saturday Morning Live session —free to register at mcdsml.com.
Thank you for listening.
