huIL5RA Mouse
Product Name
huIL5RA Mouse
Product ID
C002007
Strain Name
C57BL/6NCya-Il5ratm1(hIL5RA)/Cya
Backgroud
C57BL/6NCya
Status
When using this mouse strain in a publication, please cite “huIL5RA Mouse (Catalog C002007) were purchased from Cyagen.”
Product Type
Age
Genotype
Sex
Quantity
Gene Name
IL5RA
Gene Alias
IL5R, CD125, CDw125, HSIL5R3
NCBI ID
Chromosome
Chr 3 (Human)
MGI ID
Datasheet
Strain Description
The IL5RA gene encodes the interleukin-5 receptor subunit alpha (IL5RA), the receptor subunit that specifically binds IL5. It is primarily expressed on eosinophils, basophils, and their progenitor cells, with low expression levels in most normal tissues [1]. IL5RA plays a critical role in the proliferation, differentiation, survival, recruitment, and activation of eosinophils. Upon binding to IL5, it activates downstream signaling pathways such as JAK2-STAT5, thereby promoting type 2 inflammatory responses. Excessive activation of the IL5/IL5RA axis in cells or tissues can lead to eosinophil expansion and tissue infiltration, exacerbating inflammation and tissue damage [2]. IL5RA exerts a central regulatory role in the pathogenesis of eosinophil-related inflammatory diseases, including severe eosinophilic asthma (SEA), chronic rhinosinusitis with nasal polyps (CRSwNP), and eosinophilic granulomatosis with polyangiitis (EGPA) [3-5]. Studies have shown that abnormal IL5RA expression is causally associated with the genetic risk of multiple myeloma (MM), positioning it as a potential tumor biomarker and therapeutic target [6]. Humanized anti-IL5RA CAR-T cell therapy can effectively deplete eosinophils and their precursors at various developmental stages in the bone marrow and peripheral blood [1]. Currently, multiple clinical drugs targeting the IL-5/IL5RA pathway have been approved or are under development, including mepolizumab, reslizumab, and benralizumab [7-8].
The huIL5RA mouse was generated by replacing the mouse Il5ra endogenous extracellular domain with the human IL5RA extracellular domain. The murine transmembrane-cytoplasmic region was preserved. huIL5RA mice can be used for the research and development as well as preclinical pharmacological and efficacy evaluation of IL5RA-targeted drugs for multiple eosinophil-related inflammatory diseases, including severe eosinophilic asthma (SEA), chronic rhinosinusitis with nasal polyps (CRSwNP), and eosinophilic granulomatosis with polyangiitis (EGPA), as well as multiple myeloma (MM).
Reference
Wu Y, Zhang R, Sun B, et al. IL-5 CAR-T cell therapy induces effective remission in hypereosinophilic disorders. J Hematol Oncol. 2026;19(1):18.
Chen S, Chen G, Xu F, et al. Treatment of allergic eosinophilic asthma through engineered IL-5-anchored chimeric antigen receptor T cells. Cell Discov. 2022;8(1):80.
Buchheit KM, Shaw D, Chupp G, et al. Interleukin-5 as a pleiotropic cytokine orchestrating airway type 2 inflammation: Effects on and beyond eosinophils. Allergy. 2024;79(10):2662-2679.
Hanania NA, Herth FJF. Persistent airway obstruction in severe eosinophilic asthma: targeting interleukin-5 and eosinophils. Eur Respir Rev. 2025;34(178):250024.
Bettiol A, Urban ML, Padoan R, et al. Benralizumab for eosinophilic granulomatosis with polyangiitis: a retrospective, multicentre, cohort study. Lancet Rheumatol. 2023;5(12):e707-e715.
Went M, Duran-Lozano L, Halldorsson GH, et al. Deciphering the genetics and mechanisms of predisposition to multiple myeloma. Nat Commun. 2024;15(1):6644.
Lombardi C, Comberiati P, Ridolo E, et al. Anti-IL-5 Pathway Agents in Eosinophilic-Associated Disorders Across the Lifespan. Drugs. 2024;84(6):661-684.
Fricker M, Harrington J, Hiles SA, Gibson PG. Mepolizumab depletes inflammatory but preserves homeostatic eosinophils in severe asthma. Allergy. 2024;79(11):3118-3128.
Strain Strategy
The mouse Il5ra endogenous extracellular domain was replaced with the human IL5RA extracellular domain. The murine transmembrane-cytoplasmic region was preserved.
Figure 1. Gene editing strategy of huIL5RA mice.
Application Area
Screening, development, and preclinical evaluation of IL-5RA-targeted drugs;
Mechanistic studies of chronic rhinosinusitis with nasal polyps (CRSwNP);
Mechanistic studies of severe eosinophilic asthma (SEA);
Mechanistic studies of eosinophilic granulomatosis with polyangiitis (EGPA);
Mechanistic studies of allergic inflammation;
In vivo validation of immunotherapies;
Research on cytokine signaling pathways.
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