B6-hIL31RA Mouse
Product Name
B6-hIL31RA Mouse
Product ID
C001917
Strain Name
C57BL/6NCya-Il31raem1(hIL31RA)/Cya
Backgroud
C57BL/6NCya
Status
When using this mouse strain in a publication, please cite “B6-hIL31RA Mouse (Catalog C001917) were purchased from Cyagen.”
Product Type
Age
Genotype
Sex
Quantity
Gene Name
Gene Alias
CRL, GPL, CRL3, GLMR, GLM-R, PLCA2, hGLM-R, IL-31RA, PRO21384, zcytoR17
NCBI ID
Chromosome
Chr 5
MGI ID
Datasheet
Strain Description
The IL31RA gene encodes the interleukin-31 receptor subunit alpha, a type I cytokine receptor that serves as a critical mediator in neuroimmune communication. The protein typically functions as a heterodimer by associating with the oncostatin M receptor (OSMRβ) to form the functional IL-31 receptor complex, which triggers intracellular signaling through the JAK/STAT (primarily STAT3), PI3K/AKT, and MAPK pathways [1]. While the gene is expressed at low levels across various tissues, including the testis, thymus, and bone marrow, it is highly localized and functionally significant in CD14+ monocytes, macrophages, keratinocytes, and a specific subset of dorsal root ganglia (DRG) neurons. In these tissues, IL31RA plays a pivotal role in mediating pruritus (itching) and regulating skin immunity and inflammation [2]. Genetically, dysregulation of the IL31RA pathway is heavily implicated in the pathogenesis of inflammatory and pruritic diseases such as atopic dermatitis, prurigo nodularis, allergic asthma, and certain cutaneous T-cell lymphomas, making it a major therapeutic target for monoclonal antibodies like nemolizumab [3].
The B6-hIL31RA mouse is a humanized model constructed through gene-editing technology, in which the sequences from aa.19 to partial intron 4 of mouse Il31ra were deleted, and the human IL31RA extracellular domain-mouse Il31ra transmembrane-cytoplasmic domain-3’UTR of mouse Il31ra WPRE-BGH pA cassette was inserted downstream of mouse Il31ra signal peptide. This model can be used for research on inflammatory and pruritic diseases such as atopic dermatitis, prurigo nodularis, allergic asthma, and certain cutaneous T-cell lymphomas, as well as for screening, development, and preclinical evaluation of IL31RA-targeted therapeutics.
Reference
Suehiro M, Numata T, Saito R, Yanagida N, Ishikawa C, Uchida K, Kawaguchi T, Yanase Y, Ishiuji Y, McGrath J, Tanaka A. Oncostatin M suppresses IL31RA expression in dorsal root ganglia and interleukin-31-induced itching. Front Immunol. 2023 Nov 16;14:1251031.
Furue M, Furue M. Interleukin-31 and Pruritic Skin. J Clin Med. 2021 Apr 28;10(9):1906.
Orfali RL, Aoki V. Blockage of the IL-31 Pathway as a Potential Target Therapy for Atopic Dermatitis. Pharmaceutics. 2023 Feb 8;15(2):577.
Strain Strategy
The sequences from aa.19 to partial intron 4 of mouse Il31ra were deleted, and the human IL31RA extracellular domain-mouse Il31ra transmembrane-cytoplasmic domain-3’UTR of mouse Il31ra WPRE-BGH pA cassette was inserted downstream of mouse Il31ra signal peptide.
Figure 1. Diagram of the gene editing strategy for the generation of B6-hIL31RA mice.
Application Area
Screening, development, and pre-clinical evaluation of IL31RA-targeted drugs;
Research on the pathogenic mechanisms and relevant treatment methods of inflammatory and pruritic diseases such as atopic dermatitis, prurigo nodularis, allergic asthma, and certain cutaneous T-cell lymphomas.
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