FULL SUPPLEMENT: The Role of IL 31 Inhibition in Atopic Dermatitis

September 2026 | Volume 25 | Issue 9 | 154710s1 | Copyright © September 2026


Published online August 31, 2026

ET AL

Abstract
Atopic dermatitis and prurigo nodularis represent the two most burdensome pruritic inflammatory skin diseases encountered in clinical dermatology. While distinct in morphology, chronicity, and epidemiology, both conditions are united by a common pathophysiologic axis: type 2 immune dysregulation, peripheral neuronal sensitization, collagen deposition resulting in lichenification or nodule formation, and the relentless itch-scratch cycle that profoundly impairs quality of life. At the molecular center of this axis sits interleukin-31, a cytokine that has earned the designation "the itchy cytokine" for its potent, direct pruritogenic activity.
In this issue:

Interleukin-31 in Atopic Dermatitis and Prurigo Nodularis: Pathophysiology, Neuroimmune Mechanisms, and Clinical Efficacy of Nemolizumab
This manuscript provides an integrated review of IL-31 pathophysiology in AD and PN and the clinical efficacy of nemolizumab across both indications, with attention to skin clearance, pruritus control, sleep restoration, long-term durability, and translational biomarker insights.

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