Mouse Interleukin IL-31
- Known as:
- Mouse Interleukin Interleukin-31
- Catalog number:
- GEM-300-359P1
- Product Quantity:
- 1 mg
- Category:
- -
- Supplier:
- SeraLab
- Gene target:
- Mouse Interleukin IL-31
Related genes to: Mouse Interleukin IL-31
- 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: Mouse Interleukin IL-31
Related articles to: Mouse Interleukin IL-31
- 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 - Hyper-IgE syndrome (HIES) is characterized by recurrent infections, severe eczema, impaired inflammation, and extrahematopoietic manifestations. Most patients carry dominant-negative variants, which impair IL-6 family cytokine signaling. In this News & Views, we discuss two studies reporting autosomal recessive (AR) OSMRβ deficiency as a new inborn error of immunity. All 11 patients had severe atopy, hyper-IgE, and eosinophilia; one also had HIES-like infections and extrahematopoietic features. OSMRβ (encoded by ) and gp130 form the OSM receptor II (LIFR and gp130 form OSMR I), while OSMRβ and IL-31RA form the IL-31 receptor. Patients' variants impair OSM-induced STAT activation; IL-31 signaling was not tested. It was reported that AR OSM deficiency causes bone marrow failure, while an IL-31RA-blocking antibody improves atopic dermatitis. The respective contributions of altered OSM and IL-31 signaling to atopy in AR OSMRβ deficiency remain unresolved. These findings expand the genetic dissection of the STAT3-HIES spectrum. AR OSMRβ deficiency should be considered in patients with one or more HIES-like features. - Source: PubMed
Publication date: 2026/08/19
Puel AnneCasanova Jean-LaurentBéziat Vivien - Prurigo nodularis is a chronic pruritic dermatosis often resistant to standard therapies. We report a patient with prurigo nodularis complicated by meralgia paresthetica who achieved complete and durable resolution of pruritus after a single loading dose of nemolizumab, an interleukin-31 receptor A (IL-31RA) antagonist. This case underscores the rapid efficacy of IL-31 blockade and highlights potential neuroimmune interplay in chronic itch disorders. - Source: PubMed
Publication date: 2025/12/29
Cho Seo WonChen HelenChen AaronSontam TarunTarbox Michelle - Chronic pruritus is a common and difficult-to-manage feature of inflammatory skin conditions. It develops through complex interactions between the skin barrier, immune system, and peripheral nervous system. Interleukin-31 (IL-31) and oncostatin M (OSM), both members of the interleukin-6 (IL-6) cytokine family, share the same receptor subunit, OSM receptor β (OSMRβ), and activate common downstream intracellular pathways, particularly the Janus kinase-signal transducer and activator of transcription (JAK-STAT) cascade. This systematic review aims to synthesize evidence in the current literature that supports IL-31 and OSM signaling across chronic pruritic dermatoses, with an emphasis on downstream JAK1-STAT3 pathways. A comprehensive search was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines using PubMed, Embase, Ovid MEDLINE, and the Web of Science databases. Studies evaluating OSM, IL-31, their shared receptor components (IL-31 receptor A (IL-31RA) and OSMRβ), and downstream intracellular signaling in chronic pruritic dermatoses were included. Twenty-six studies met the eligibility criteria, comprising randomized controlled trials, case-control studies, cross-sectional studies, case series, and experimental laboratory studies. Across atopic dermatitis (AD), prurigo nodularis (PN), psoriasis, cutaneous T-cell lymphoma (CTCL), dermatomyositis, and primary localized cutaneous amyloidosis (PLCA), both IL-31 and OSM contribute to chronic itch through overlapping pathways, including shared receptor architecture and activation of JAK1-STAT3 signaling. They were found to differ, however, in the way they influence neuronal activation and sensitization. IL-31 acts as a direct pruritogenic cytokine through activation of the IL-31RA/OSMRβ receptor complex on sensory neurons. In contrast, OSM may act to increase neuronal sensitivity, enhance excitability, and strengthen the response to other pruritic-inducing stimuli through the gp130/OSMRβ receptor complex. Despite these differences, both cytokines converge on the JAK1-driven STAT3 signaling pathway, ultimately contributing to skin barrier dysfunction, ongoing inflammation, and persistent neural sensitization. Blocking IL-31RA with nemolizumab or targeting OSMRβ with vixarelimab has led to clinically significant improvements in itch severity, patient-reported quality of life, and sleep disturbance. Together, these findings suggest that the shared components of the IL-31 and OSM pathways, including OSMRβ and JAK1-STAT3, provide us with a big picture framework for understanding itch pathogenesis in chronic pruritic dermatoses and may help guide therapeutic strategies in the future. - Source: PubMed
Publication date: 2026/04/29
Tashjian MichelleRankin Erica KTehrani LilyRuppe MarissaRiskin Suzanne I