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)
- 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 - Oncostatin M receptor beta (OSMRβ) is an essential signal-transducing subunit in the IL-31/IL-31 receptor alpha (IL-31RA)/OSMRβ complex and is implicated in inflammatory and pruritic diseases. We previously developed a high-affinity monoclonal antibody (2O2) that targets the proximal extracellular domain (amino acids 619-734) of canine OSMRβ (cOSMRβ) and shows no cross-reactivity with human OSMRβ (hOSMRβ). Here, we elucidate its functional mechanism of action and determine the co-crystal structure of the 2O2 Fab fragment in complex with this domain at a resolution of 2.76 Å. Consistent with the epitope location far away from the cytokine-binding domain (CBD) of cOSMRβ, 2O2 does not compete with canine IL-31 (cIL-31) for cOSMRβ binding. However, the in vitro functional assay demonstrated that 2O2 inhibits cIL-31-induced phosphorylation of STAT5 in DH-82 cells. Mechanistically, this inhibition is achieved through antibody-induced internalization of cOSMRβ from the cell surface. Structural analysis reveals that 2O2 binds at an oblique angle relative to the membrane, creating steric hindrance that induces localized lipid bilayer invagination. The bivalent IgG exhibits ∼34-fold higher potency than its monovalent Fab, reflecting not only avidity but also mechanical consequences of dual receptor engagement: crosslinking two receptor complexes exerts a stretching force that amplifies membrane invagination and promotes efficient endocytic uptake. This mechanism enables clearance of the entire signaling complex, including the cytokine, from the cell surface-a functional advantage over conventional cytokine-blocking antibodies. These findings establish 2O2 as a novel canine therapeutic candidate with a distinct internalization-driven mechanism of action. - Source: PubMed
Publication date: 2026/06/01
Zhang CailiGuo TianlingZheng YuxinPang XuefeiWang LixianLi YuGao FengXiao Haixia - Oncostatin M (OSM) receptor beta (OSMRβ), encoded by , is a cytokine receptor subunit required for signaling by OSM and IL-31. We identified 10 affected individuals from seven unrelated families with germline biallelic loss-of-function variants in who shared a phenotype of early-onset, severe, widespread atopic dermatitis with peripheral eosinophilia and markedly elevated serum IgE. All patient-derived OSMRβ variants failed to localize to the cell surface, resulting in selective loss of OSM-dependent signaling. Patient cells showed markedly reduced OSM-induced phosphorylation of STAT1, STAT3, and STAT5, while signaling through other IL-6 family receptor complexes remained intact. Transcriptomic profiling of patient primary dermal fibroblasts revealed consistent downstream effects, including loss of interferon-responsive and inflammatory gene programs. Re-expression of wild-type restored receptor surface expression, STAT activation, and transcriptional responses, confirming a causal loss-of-function mechanism. Together, these findings establish biallelic deficiency as a novel primary atopic disorder. - Source: PubMed
Publication date: 2026/05/28
Samra SimranSharma MehulKörholz JuliaLiu YihuiJames AlyssaMichalski ChristinaYousefi PariyaDel Bel Kate LLu Henry YSharma Ashish ATarailo-Graovac MajaDalmann JoshuaBuder LilyModi BhaviWiedemuth RalfGolding LiamDrögemöller BrittBlanchard-Rohner GéraldineSenger ChristofRehmus WingfieldPrendiville Julie SMangino MassimoRoss Colin Jvan Karnebeek Clara D MWasserman Wyeth WD Rosenzweig SergioNiemela JulieLavoie Pascal MPrathibha P MWegehaupt OliverBiggs Catherine MBoehnke MichaelKinnunen LeenaKoistinen Heikki AMcKinnon Margaret LBreuer Jonas MaximillianSchönenkorb JanaBrock RobertThull SarahNetzer ChristianVelmans ClaraAltuwaijri NorahHamadah Issam RAltassan RuqaiahAlfares AhmedMaddirevula SateeshPatil Siddaramappa JagdishBayer Diana KLyons Jonathan JTurvey Stuart E - 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 - Atopic dermatitis is a heterogeneous inflammatory skin disease long-defined by skin barrier dysfunction and type 2 (T helper cell [Th]2) immune dysregulation. Dupilumab established interleukin (IL)-4 and IL-13 as key therapeutic targets, yet partial response rates underscore contributions from Th1, Th17, Th22, and other pathways that vary by age, ethnicity, and disease stage. Cytokine signaling convergence through the Janus kinase/signal transducers and activators of transcription axis underlies the broad efficacy of oral Janus kinase inhibitors, while persistence of tissue-resident memory T cells in clinically resolved skin highlights the role of immune memory and supports therapeutic strategies targeting OX40/OX40L. The neuroimmune axis, exemplified by IL-31 signaling and keratinocyte-neuron crosstalk, drives pruritus and perpetuates local inflammation. Additionally, keratinocyte dysregulation and lipid abnormalities perpetuate barrier defects, while impaired antimicrobial defenses permit Staphylococcus aureus overgrowth and further skew immunity. Emerging therapies, including IL-22, IL-31, IL-18, OX40 pathway inhibitors, and AhR agonists, continue to expand opportunities for individualized treatment of atopic dermatitis. Together, these advances emphasize atopic dermatitis as a systemic, relapsing disease caused and sustained by simultaneous immunologic, barrier, microbial, and neural dysregulation. A deeper mechanistic understanding will lead to long-term disease modification and relief. - Source: PubMed
Zhou JerryFiedler JacobGuttman-Yassky Emma