Ask about this productRelated genes to: IL31 protein
- 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
Related articles to: IL31 protein
- Bullous pemphigoid (BP) is a chronic autoimmune blistering disease predominantly affecting the elderly, with conventional immunosuppressive treatments often limited by insufficient efficacy and severe adverse effects. Emerging targeted therapies offer new opportunities, yet optimal treatment strategies remain to be defined. Herein, we report a case of BP in a 69-year-old woman with insufficient response to initial systemic corticosteroid therapy, successfully managed with a bridging targeted approach using abrocitinib and dupilumab. Initiation of abrocitinib (200 mg daily) resulted in rapid pruritus relief within 24 hours and cessation of new blister formation within 6 days. Symptom relapse and reinduction upon dose reduction and restoration suggested a dose-dependent therapeutic effect of abrocitinib. Dupilumab was subsequently introduced for long-term disease control, while abrocitinib was gradually tapered off. After more than six months of targeted therapy, sustained complete remission was achieved, with a favorable safety profile. Objective disease activity improved in parallel with clinical remission, with BPDAI decreasing from 120 at baseline to 0, pruritus NRS from 9 to 0, and peripheral eosinophil counts returning to the normal range during follow-up. Mechanistically, abrocitinib may rapidly suppress pruritus and inflammation through JAK1-dependent blockade of IL-4, IL-13, and IL-31 signaling. In contrast, dupilumab provides sustained disease control by inhibiting IL-4/IL-13-mediated Th2 responses, reducing eosinophilic inflammation and autoantibody production. This case highlights a complementary therapeutic strategy integrating rapid disease control with long-term immune modulation, suggesting that our bridging therapy may represent a rational and effective approach for patients with bullous pemphigoid with insufficient response to initial corticosteroid therapy, warranting further investigation in controlled studies. - Source: PubMed
Publication date: 2026/08/24
Zhang HongchanLi LinqiZhao SusuWu HaoZhu Jianwei - The autoimmune regulator (Aire) gene is essential for the establishment of central tolerance by promoting the ectopic expression of tissue-restricted antigens in medullary thymic epithelial cells (mTECs). Although Aire deficiency impairs negative selection, its impact on thymic architecture, output, and early T cell development remains incompletely understood. Here, we used a murine Aire-deficient model carrying a CRISPR-Cas9-induced deletion within exon 6, disrupting the SAND domain, to investigate the consequences of Aire loss on thymic structure and function. Aire-deficient mice exhibited focal alopecia and marked disorganization of the thymic medulla. T cell receptor excision circle (TREC) analyses revealed altered peripheral TREC dynamics and a reduced sj/betaTREC ratio, indicating altered thymic output and impaired intrathymic precursor expansion. Complementary flow-cytometric analysis showed a significant reduction in the proportion of CD4CD8 double-positive thymocytes in heterozygous mutants, supporting altered intrathymic maturation. Serum IL-27, IL-28B, and IL-31 were decreased in homozygous mutants, whereas IL-22 and IL-23 remained unchanged. Despite these alterations, TCRVbeta repertoire sequencing revealed no significant differences in rearrangements, clonality, or V/J gene usage. Together, these findings indicate that Aire deficiency disrupts thymic architecture and output, while preserving overall TCR repertoire diversity. - Source: PubMed
Publication date: 2026/09/06
Matos Adriana ArrudaAraujo Itauá LestonMunuera Matheus DominatoPalma Patrícia Viana BoniniBonaldo CamilaBrito Letícia AgrelliMendes-da-Cruz Daniella ArêasSavino WilsonPassos Geraldo AleixoDonadi Eduardo Antônio - 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