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Last update 08 May 2025

IL-31RB

Last update 08 May 2025

Basic Info

Synonyms

IL-31 receptor subunit beta, IL-31R subunit beta, IL-31R-beta

+ [7]

Introduction

Associates with IL31RA to form the IL31 receptor. Binds IL31 to activate STAT3 and possibly STAT1 and STAT5. Capable of transducing OSM-specific signaling events.

Drugs associated with IL-31RB

Vixarelimab

Target

IL-31RB

Mechanism

OSMRβ inhibitors

Active Org.

Genentech, Inc. [+2]

Originator Org.

Biogen, Inc.

Active Indication

Colitis, Ulcerative [+4]

Inactive Indication

Chronic Disease [+4]

Drug Highest PhasePhase 2

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Anti-OSMR antibody-gold nanorods(BYU)

Target

IL-31RB

Mechanism

OSMRβ inhibitors

Active Org.

Brigham Young University

Originator Org.

Brigham Young University

Active Indication

Synovial Sarcoma

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with IL-31RB

NCT06693908

/ RecruitingPhase 1/2

A Phase Ic Open-label Study to Evaluate the Pharmacodynamic Effects, Pharmacokinetics, and Safety of Vixarelimab in Patients With Moderate to Severe Active Ulcerative Colitis

This study aims to evaluate the pharmacodynamic (PD) effects of vixarelimab in the gut of participants with active moderate to severe ulcerative colitis (UC).

Start Date31 Mar 2025

Sponsor / Collaborator

Genentech, Inc.

CTIS2024-516287-29-00

/ RecruitingPhase 1

- GA45735

Start Date11 Mar 2025

Sponsor / Collaborator

Genentech, Inc.

NCT06137183

/ Active, not recruitingPhase 2

A Phase II, Multicenter Induction Study With an Active Treatment Extension to Evaluate the Efficacy, Safety, and Pharmacokinetics of Vixarelimab in Patients With Moderate to Severe Ulcerative Colitis

The purpose of this study is to evaluate the efficacy, safety, and pharmacokinetics (PK) of vixarelimab compared with placebo in participants with moderate to severe UC who have demonstrated inadequate response to, loss of response to, or intolerance to prior conventional or advanced therapy.

Start Date01 May 2024

Sponsor / Collaborator

Genentech, Inc.

100 Clinical Results associated with IL-31RB

100 Translational Medicine associated with IL-31RB

0 Patents (Medical) associated with IL-31RB

398

Literatures (Medical) associated with IL-31RB

01 Apr 2025·Journal of Allergy and Clinical Immunology

Nasal transcriptome differences preceding recurrent wheezing in infancy

Article

Author: Dhar, Poshmaal ; Morgan, Rachel ; Ashley, Sarah ; Vuillermin, Peter ; Saffery, Richard ; Ponsonby, Anne-Louise ; Collier, Fiona ; O'Hely, Martin ; Mansell, Toby ; Sly, Peter D ; Ranganathan, Sarath C ; Burgner, David ; Tang, Mimi Lk ; Sominsky, Luba

BACKGROUNDMucosal immune responses and epithelial barrier function are key emerging determinants of susceptibility to wheezing illnesses in early life.OBJECTIVEWe investigated the association between nasal transcriptome in healthy infants and the subsequent incidence of recurrent wheeze.METHODSIn a population-derived prebirth cohort study, whole transcriptome sequencing was performed to compare the nasal transcriptome at 1 month of age from 26 infants who subsequently developed recurrent wheeze (parents' record in symptom diary) in the first year of life to 22 infants who remained recurrent wheeze-free. Differentially expressed genes (DEGs) were identified using DEseq2, followed by over-representation pathway (GO and KEGG) and upstream regulator analyses (Ingenuity Pathway Analysis).RESULTS202 DEGs (false discovery rate ≤ 0.1 and absolute log₂ fold change > 1; 66 upregulated and 136 downregulated) were associated with recurrent wheeze. Upregulated GO pathways associated with recurrent wheeze included chemokine-mediated signalling, eosinophil and monocyte chemotaxis. The downregulated GO included cilium organisation and cellular aldehyde metabolic process. TNF emerged as the key driver (adjusted p-value and Z-score) of DEG patterns in the recurrent wheeze group, with OSMR and IL21 identified as master regulators.CONCLUSIONThe nasal transcriptome in early infancy is associated with subsequent recurrent wheezes, indicating upregulation of immune cell chemotaxis, decreased epithelial barrier function, and altered cilium organisation and mitochondrial function. Future studies are required to evaluate the use of nasal transcriptome in the early detection of infants at risk of recurrent wheeze and to generate new knowledge of antecedent pathways as targets for novel primary prevention strategies.

17 Mar 2025·Journal of Clinical Investigation

Human oncostatin M deficiency underlies an inherited severe bone marrow failure syndrome

Article

Author: Mahony, Christopher B ; Willems, Marjolaine ; Cavazzana, Marina ; Anginot, Adrienne ; Susini, Sandrine ; Garrigue, Alexandrine ; Callebaut, Isabelle ; Cormier-Daire, Valérie ; Kermasson, Laëtitia ; Luce, Sonia ; Fert, Ingrid ; Le Bousse-Kerdilès, Marie-Caroline ; Bertrand, Julien Y ; Six, Emmanuelle ; Chouteau, Myriam ; André, Isabelle ; Sirvent, Anne ; Lagresle-Peyrou, Chantal ; Sadek, Hanem ; Souraud, Jean-Baptiste ; Revy, Patrick ; Russello, Jennifer

Oncostatin M (OSM) is a cytokine with the unique ability to interact with both the OSM receptor (OSMR) and the leukemia inhibitory factor receptor (LIFR). On the other hand, OSMR interacts with IL31RA to form the interleukin-31 receptor. This intricate network of cytokines and receptors makes it difficult to understand the specific function of OSM. While monoallelic loss-of-function (LoF) mutations in OSMR underlie autosomal dominant familial primary localized cutaneous amyloidosis, the in vivo consequences of human OSM deficiency have never been reported so far. Here, we identified 3 young individuals from a consanguineous family presenting with inherited severe bone marrow failure syndromes (IBMFS) characterized by profound anemia, thrombocytopenia, and neutropenia. Genetic analysis revealed a homozygous 1 base-pair insertion in the sequence of OSM associated with the disease. Structural and functional analyses showed that this variant causes a frameshift that replaces the C-terminal portion of OSM, which contains the FxxK motif that interacts with both OSMR and LIFR, with a neopeptide. The lack of detection and signaling of the mutant OSM suggests a LoF mutation. Analysis of zebrafish models further supported the role of the OSM/OSMR signaling in erythroid progenitor proliferation and neutrophil differentiation. Our study provides the previously uncharacterized and unexpectedly limited in vivo consequence of OSM deficiency in humans.

01 Jan 2025·CNS Neuroscience & Therapeutics

A Risk Model Based on Ferroptosis‐Related Genes OSMR, G0S2, IGFBP6, IGHG2, and FMOD Predicts Prognosis in Glioblastoma Multiforme

Article

Author: Wu, Yaqiu ; Li, Zhili ; Liu, Ling ; Wang, Qi ; Cheng, Meixiong ; Zhang, Tian

ABSTRACTBackgroundGlioblastoma multiforme (GBM) is a common and highly aggressive brain tumor with a poor prognosis. However, the prognostic value of ferroptosis‐related genes (FRGs) and their classification remains insufficiently studied.ObjectiveThis study aims to explore the significance of ferroptosis classification and its risk model in GBM using multi‐omics approaches and to evaluate its potential in prognostic assessment.MethodsFerroptosis‐related genes (FRGs) were retrieved from databases such as FerrDB. The TCGA‐GBM and CGGA‐GBM datasets were used as training and testing cohorts, respectively. Univariate Cox regression and LASSO regression analyses were performed to establish a risk model comprising five genes (OSMR, G0S2, IGFBP6, IGHG2, FMOD). A Meta‐analysis of integrated TCGA and GTEx data was conducted to examine the differential expression of these genes between GBM and normal tissues. Key gene protein expression differences were analyzed using CPTAC and HPA databases. Single‐cell RNA sequencing (scRNA‐seq) analysis was employed to explore the cell type‐specific distribution of these genes.ResultsThe five‐gene risk model demonstrated significant prognostic value in GBM. Meta‐analysis revealed distinct expression patterns of the identified genes between GBM and normal tissues. Protein expression analysis confirmed these differences. scRNA‐seq analysis highlighted the diverse distribution of these genes across different cell types, offering insights into their biological roles.ConclusionThe ferroptosis‐based risk model provides valuable prognostic insights into GBM and highlights potential therapeutic targets, emphasizing the biological significance of ferroptosis‐related genes in tumor progression.

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