Ask about this productRelated genes to: IL31 protein (Mouse)
- Gene:
- IL31 NIH gene
- Name:
- interleukin 31
- Previous symbol:
- -
- Synonyms:
- IL-31
- Chromosome:
- 12q24.31
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-06
- Date modifiied:
- 2014-11-19
Related products to: IL31 protein (Mouse)
Related articles to: IL31 protein (Mouse)
- Chronic cough, a distressing symptom of allergic asthma, possibly arises from the abnormal activation of airway-projecting sensory neurons. Levels of interleukin (IL)-31, a Th2 cytokine known for its neuronal effects in pruritus, are elevated in allergic disorders; however, its role in asthma-related cough remains unclear. Therefore, in this study, we aimed to determine the mechanism by which IL-31 influences cough-associated neuronal sensitization using a Dermatophagoides farinae (Derf)-induced asthma model. - Source: PubMed
Miyamoto TakayoshiOhira ChiharuKaneki MaoKomuro MarikoIchikawa ManaYasuda IbukiTakagi YoshiichiFukuyama Tomoki - Interleukin-31 (IL-31) is a central mediator in atopic dermatitis (AD) and prurigo nodularis (PN), functioning both as the principal pruritogenic cytokine, driving itch through direct neuronal activation via the IL-31RA/OSMRβ signaling axis, and as a key immunological amplifier that sustains Th2 polarization by promoting continued IL-4 and IL-13 production. Beyond these neuroimmune effects, IL-31 disrupts epidermal barrier integrity and acts directly on dermal fibroblasts to drive collagen synthesis and extracellular matrix remodeling, contributing to the lichenification of chronic AD and the hyperkeratotic nodule formation that defines PN. This narrative review integrates the mechanistic biology of IL-31 across both conditions with the clinical evidence base for nemolizumab, a humanized monoclonal antibody targeting IL-31RA, examining phase 3 trial data, long-term extension outcomes, translational biomarker evidence, and emerging real-world experience. - Source: PubMed
Issa Naiem TKwatra ShawnShahbaz AliKircik Leon - Atopic dermatitis (AD) is characterized by pruritus, epidermal hyperplasia, and lichenification that significantly impairs quality of life. Nemolizumab, an anti-IL-31Rα monoclonal antibody, is approved for treating moderate-to-severe AD in patients aged > 12 years. This study investigated nemolizumab's molecular mechanisms using patient samples from the ARCADIA 1 (NCT03985943) and 2 (NCT03989349) trials. - Source: PubMed
Publication date: 2026/09/04
Liu DanielDuca Ester DelDelaleu NicolasLau MeganPulsinelli Julianade Rosa Joel CorreaBar JonathanEstrada YerielGudjonsson JohannJulia ValerieGuttman-Yassky Emma - Managing pruritus in hemodialysis patients is challenging. Nemolizumab, a monoclonal antibody targeting IL-31, has demonstrated efficacy in atopic dermatitis and prurigo nodularis with fast reduction of pruritus. - Source: PubMed
Publication date: 2026/09/01
Mathur Vandana SFishbane StevenStänder SonjaSzepietowski Jacek CHernandez German TJamal AamirLynn RobertRossini MatteoZhu JuliePiketty ChristopheYosipovitch Gil - Type 2 inflammation is a fundamental immunologic pathway underlying a growing spectrum of dermatologic diseases. While classically associated with atopic dermatitis, type 2 immune responses are increasingly recognized as key contributors to prurigo nodularis, chronic spontaneous urticaria, bullous pemphigoid, lichen simplex chronicus, and other chronic pruritic disorders. Barrier disruption and epithelial injury initiate the release of alarmins, including thymic stromal lymphopoietin (TSLP), interleukin (IL)-33, and IL-25, which activate innate and adaptive immune pathways that promote type 2 inflammation. Subsequent production of effector mediators such as IL-4, IL-13, IL-5, IL-31, immunoglobulin E (IgE), and periostin drives barrier dysfunction, immune cell recruitment, tissue remodeling, and chronic pruritus. Increasing evidence further highlights the importance of neuroimmune crosstalk, with direct interactions between immune cells, cytokines, and sensory neurons contributing to itch sensitization and disease persistence. The clinical success of biologic therapies targeting IL-4/IL-13, IgE, and IL-31 signaling has provided powerful functional validation of these pathogenic pathways and has transformed the management of multiple inflammatory skin diseases. In this review, we summarize the molecular and cellular mechanisms underlying type 2 inflammation in the skin, discuss its role across diverse dermatologic conditions, and highlight emerging concepts in disease heterogeneity, neuroimmune signaling, and precision medicine. Collectively, these findings support type 2 inflammation as a unifying immunologic framework and therapeutically actionable target across dermatology. - Source: PubMed
Publication date: 2026/08/17
Khalil NicoleFarhadi LeahYosipovitch Gil