Why target IL-31 for itch?
This review argues IL-31/IL-31R drive pruritus across skin diseases and highlights nemolizumab as the late-stage antibody against the IL-31 receptor.
Source
Interleukin-31 as a Clinical Target for Pruritus Treatment
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Why target IL-31 for itch?
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IL-31 was first identified in 2004.
The T-cell-derived cytokine interleukin-31 (IL-31) was first identified in 2004
Therapeutic rationale?
both IL-31 and its receptor have become potential therapeutic targets for a range of pruritic diseases
What they did
Synthesized evidence that IL-31 (identified 2004) and its receptor contribute to itch and barrier/inflammatory signs, summarizing elevated IL-31 signaling in atopic dermatitis, prurigo nodularis, and psoriasis and surveying emerging anti-IL-31 strategies.
What they found
Elevated IL-31 or receptor levels appear in multiple pruritic diseases; serum IL-31 in atopic dermatitis tracks severity/itch. Current antipruritics are often inadequate. Among pipeline agents, only nemolizumab (anti-IL-31R mAb) had successfully completed late-stage clinical studies at the time of writing.
The limits
What it doesn't show
Narrative review—not a new RCT meta-analysis; drug landscape may have changed after 2021 publication.
Key terms
- IL-31
- T-cell-derived cytokine strongly linked to pruritus.
- IL-31RA
- IL-31 receptor alpha chain targeted by some therapies.
- Pruritus
- Itch that impairs sleep, mood, and daily function.
- Nemolizumab
- Humanized mAb against the IL-31 receptor.
- Atopic dermatitis
- Common inflammatory skin disease with prominent itch.
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IL-31 was first identified in:
Common questions
When was IL-31 identified?
2004.
Diseases with elevated IL-31 signaling examples?
Atopic dermatitis, prurigo nodularis, psoriasis.
Leading late-stage agent named?
Nemolizumab (anti-IL-31 receptor).
Clinical need emphasized?
Current antipruritic treatments are often ineffective.