Mouse Interleukin IL-31
- Known as:
- Mouse Interleukin Interleukin-31
- Catalog number:
- GEM-300-359P100
- Product Quantity:
- 100 ug
- 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
- Nemolizumab, a humanized monoclonal antibody targeting interleukin-31 receptor α (IL-31Rα), is approved for atopic dermatitis (AD) and prurigo nodularis (PN) in adults and pediatric patients 12 years and older, following phase 3 trials demonstrating significant reductions in pruritus and disease severity in patients inadequately controlled with topical therapies. Emerging evidence has demonstrated rapid and sustained pruritus reduction in diverse pruritic conditions beyond its approved indications. - Source: PubMed
Feron HermonGottlieb Alice B - 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