IL-31: A new key player in dermatology and beyond

Bağcı, Işın Sinem; Ruzicka, Thomas

doi:10.1016/j.jaci.2017.10.045

Cited by 104 publications

(106 citation statements)

References 88 publications

(150 reference statements)

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“…From a broader perspective, IL-31 helps drive T H 2-associated inflammation by modulating keratinocyte differentiation and the immune response through stimulation of proinflammatory cytokines. 13 Increased skin barrier penetration of allergens and irritants has been shown to accompany IL-31-associated alteration of keratinocyte differentiation. 13 Furthermore, IL-31 can induce pathologic remodeling of the skin through increased epidermal basal cell proliferation, leading to epidermal thickening, and stimulated transepidermal water loss and additional impaired skin barrier function.…”

Section: Abbreviations Usedmentioning

confidence: 99%

Phase 2B randomized study of nemolizumab in adults with moderate-to-severe atopic dermatitis and severe pruritus

Silverberg

Pinter

Pulka

et al. 2020

Journal of Allergy and Clinical Immunology

187

147

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Background: Nemolizumab targets the IL-31 receptor a subunit involved in atopic dermatitis (AD) pathogenesis. Objective: We sought to evaluate a new dosing strategy of nemolizumab in patients with AD. Methods: We performed a 24-week, randomized, double-blind, multicenter study of nemolizumab (10, 30, and 90 mg) subcutaneous injections every 4 weeks versus placebo, with topical corticosteroids in adults with moderate-to-severe AD, severe pruritus, and inadequate control with topical treatment (n 5 226). The Eczema Area and Severity Index (EASI), the peak pruritus (PP) numeric rating scale (NRS), and the Investigator's Global Assessment (IGA) were assessed. Standard safety assessments were performed. Results: Nemolizumab improved EASI, IGA, and/or NRS-itch scores, with the 30-mg dose being most effective. Nemolizumab (30 mg) reduced EASI scores versus placebo at week 24 (268.8% vs 252.1%, P 5 .016); significant differences were observed by week 8 (P < _ .01). With significant improvement (P 5 .028) as early as week 4, IGA 0/1 rates were higher for 30 mg of nemolizumab versus placebo at week 16 (33.3% vs 12.3%, P 5 .008) but not week 24 because of an increased placebo/topical corticosteroid effect (36.8% vs 21.1%, P 5 .06). PP-NRS scores were improved for 30 mg of nemolizumab versus placebo at week 16 (268.6% vs 234.3%, P < .0001) and week 24 (267.3% vs 235.8%, P < .0001), with a difference by week 1 (P < .001). NRS response rates (> _4-point decrease) were greater for 30 mg of nemolizumab versus placebo at week 16 (P < _ .001) and week 24 (P < _ .01). Nemolizumab was safe and well tolerated. The most common adverse events were nasopharyngitis and upper respiratory tract infection. Conclusions: Nemolizumab resulted in rapid and sustained improvements in cutaneous signs of inflammation and pruritus in patients with AD, with maximal efficacy observed at 30 mg. Nemolizumab had an acceptable safety profile.

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Section: Abbreviations Usedmentioning

confidence: 99%

Phase 2B randomized study of nemolizumab in adults with moderate-to-severe atopic dermatitis and severe pruritus

Silverberg

Pinter

Pulka

et al. 2020

Journal of Allergy and Clinical Immunology

187

147

View full text Add to dashboard Cite

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“…IL‐31 is implicated in various pruritic conditions . In patients with psoriasis, there are elevations of IL‐31 gene transcription and serum levels .…”

Section: Players In the “Scalp Itch Orchestra”mentioning

confidence: 99%

Itching for an answer: A review of potential mechanisms of scalp itch in psoriasis

Leon

Rosen

Hashimoto

et al. 2019

Experimental Dermatology

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Scalp psoriatic itch is a common complaint and often poses a therapeutic challenge. The pathophysiology of this phenomenon is unclear. The unique anatomy of the scalp contains richly innervated hair follicles, abundant vasculature and perifollicular inflammatory cytokines which may all contribute to this common sensory complaint. The mast cell, in particular, is portrayed as one of the main itch conductors for its ability to trigger neurogenic inflammation, activate the peripheral hypothalamic‐pituitary‐adrenal‐axis, process and integrate itch signalling through its interactions with the scalp hair follicles. Herein, we explain and speculate upon potential mechanisms underlying itchy scalp psoriasis, involving interconnections between the neuroimmune, neurovascular and neuroendocrine systems. Many factors may play roles in itchy scalp psoriasis including the scalp hair structure, immune system, endocrine system, nervous system and vascular system. These may warrant further exploration as therapeutic targets that go beyond the application of mere anti‐inflammatory agents.

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“…With the unveiling of the pathways involved in chronic prurigo, novel specific agents have been developed. For instance, interleukin 31 plays a relevant role in Th2‐mediated inflammation . A monoclonal antibody targeting the receptor A of interleukin 31 (nemolizumab) showed promising anti‐pruritic effects in patients with atopic dermatitis, while results from a phase II trial enrolling patients with chronic prurigo are pending.…”

Section: Unmet Needs and Future Perspectivesmentioning

confidence: 99%

How to define chronic prurigo?

Pereira

Ständer

2019

Experimental Dermatology

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Chronic prurigo impairs quality of life and is immensely challenging to treat. Until recently, no clear definition or classification system was available for this disease. A European task force specialized in pruritus defined chronic prurigo as a distinct disease characterized by chronic pruritus, a lengthy scratching behaviour and the presence of pruriginous lesions. Papular, nodular, plaque, umbilicated and linear prurigo were identified as clinical subtypes according to the most prominent lesion type observed in the physical examination. Various clinical and pathophysiological aspects, which are common across the range of clinical manifestations of chronic prurigo, argue for chronic prurigo as a disease in its own right. Chronic prurigo should be clearly demarcated from other conditions such as so‐called acute or subacute prurigo forms as well as from psychogenic self‐inflicted skin lesions, since different diagnostic criteria apply for these diseases. This viewpoint essay provides a detailed definition and classification of chronic prurigo including its obligatory and associated diagnostic criteria and discusses chronic prurigo as a distinct disease as well as the demarcation to other relevant conditions.

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IL-31: A new key player in dermatology and beyond

Cited by 104 publications

References 88 publications

Phase 2B randomized study of nemolizumab in adults with moderate-to-severe atopic dermatitis and severe pruritus

Phase 2B randomized study of nemolizumab in adults with moderate-to-severe atopic dermatitis and severe pruritus

Itching for an answer: A review of potential mechanisms of scalp itch in psoriasis

How to define chronic prurigo?

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