Interleukin-13, encoded by the IL13 gene, is a key type 2 immune response cytokine, predominantly expressed by activated Th2 helper T cells, type 2 innate lymphoid cells (ILC2s), and mast cells, and central to type 2 immune responses elicited by allergens or other stimuli ^[1]. The IL-13 protein, a ~13 kDa molecule with a four-helix bundle structure, mediates its biological effects by binding to the cell surface receptor IL-13Rα1 and recruiting the IL-4Rα chain to form a functional receptor complex, thereby activating the downstream JAK/STAT6 signaling pathway ^[2]. Key functions of IL-13 include promoting B cell maturation and plasma cell differentiation, inducing IgE isotype switching, and suppressing the pro-inflammatory activity of macrophages, leading to reduced production of pro-inflammatory cytokines and chemokines ^[3]. Furthermore, IL-13 induces goblet cell hyperplasia, promotes mucus secretion, and contributes to airway remodeling and fibrosis ^[4]. Numerous studies have established the critical role of IL-13 in the pathogenesis of various diseases, including asthma, allergic rhinitis, atopic dermatitis, and eosinophilic esophagitis ^[1-4]. Consequently, targeting IL-13 and its signaling pathways has become a significant therapeutic strategy for these conditions; for example, the monoclonal antibody Dupilumab, which simultaneously blocks IL-4 and IL-13 signaling, has demonstrated substantial efficacy in treating diverse type 2 inflammation-related diseases ^[5]. Thus, IL-13 represents a promising therapeutic target for allergic and inflammatory disorders. Thymic stromal lymphopoietin (TSLP), an interleukin-7 (IL-7) family cytokine, is encoded by the TSLP gene and is predominantly produced by epithelial cells. Its expression is notably upregulated by environmental cues, including allergens and proteases, positioning it as a sentinel at the interface of environmental exposure and immune activation ^[6-7]. Secreted by a range of cell types, such as epithelial cells, keratinocytes, mast cells, and dendritic cells, TSLP is critical in the initiation of immune responses, primarily through the activation of dendritic cells and subsequent polarization of T helper type 2 (Th2) cell differentiation. This process has broad implications for diverse immune cell populations and B cell functions relevant to allergic inflammation ^[7]. Transcriptional regulation of TSLP gene expression is tightly controlled by factors including NF-κB and AP-1, with genetic polymorphisms within the TSLP locus being strongly implicated in asthma susceptibility ^[6-8]. Dysregulated TSLP signaling is now recognized as a pivotal factor in the pathogenesis of atopic disorders, encompassing conditions such as atopic dermatitis, asthma, allergic rhinitis, and eosinophilic esophagitis ^[6-9]. For example, tezepelumab, a monoclonal antibody that blocks the TSLP signaling pathway, has demonstrated significant efficacy in clinical trials for patients with severe asthma, reducing acute exacerbations and improving lung function ^[9]. Consequently, TSLP is under intense investigation as a therapeutic target, with current strategies focusing on disrupting its signaling pathways to modulate allergic and inflammatory diseases. The B6-huIL13/huTSLP mouse is a double-gene humanized model obtained by mating B6-huIL13 mice (catalog number: C001634) with B6-huTSLP mice (catalog number: C001809). This model can be used for mechanism research and development of treatment methods for allergic diseases, inflammation, and autoimmune diseases, as well as for the development of IL13/TSLP-targeted drugs.

Interleukin-13, encoded by the IL13 gene, is a key type 2 immune response cytokine, predominantly expressed by activated Th2 helper T cells, type 2 innate lymphoid cells (ILC2s), and mast cells, and central to type 2 immune responses elicited by allergens or other stimuli ^[1]. The IL-13 protein, a ~13 kDa molecule with a four-helix bundle structure, mediates its biological effects by binding to the cell surface receptor IL-13Rα1 and recruiting the IL-4Rα chain to form a functional receptor complex, thereby activating the downstream JAK/STAT6 signaling pathway ^[2]. Key functions of IL-13 include promoting B cell maturation and plasma cell differentiation, inducing IgE isotype switching, and suppressing the pro-inflammatory activity of macrophages, leading to reduced production of pro-inflammatory cytokines and chemokines ^[3]. Furthermore, IL-13 induces goblet cell hyperplasia, promotes mucus secretion, and contributes to airway remodeling and fibrosis ^[4]. Numerous studies have established the critical role of IL-13 in the pathogenesis of various diseases, including asthma, allergic rhinitis, atopic dermatitis, and eosinophilic esophagitis ^[1-4]. Consequently, targeting IL-13 and its signaling pathways has become a significant therapeutic strategy for these conditions; for example, the monoclonal antibody Dupilumab, which simultaneously blocks IL-4 and IL-13 signaling, has demonstrated substantial efficacy in treating diverse type 2 inflammation-related diseases ^[5]. Thus, IL-13 represents a promising therapeutic target for allergic and inflammatory disorders. The IL23A gene encodes the p19 subunit, a component of interleukin-23 (IL-23), which forms a heterodimer with the p40 subunit (encoded by IL12B) to generate the functional IL-23 cytokine. Primarily expressed by activated dendritic cells, macrophages, and monocytes, IL-23 signals through the IL-23 receptor (IL-23R) complex, activating the JAK-STAT pathway to promote Th17 cell differentiation and maintain IL-17 production. This process drives inflammatory responses and mucosal immunity against extracellular pathogens ^[6-7]. Genetic polymorphisms within IL23A are strongly associated with autoimmune and inflammatory diseases, including psoriasis, Crohn's disease, and inflammatory bowel disease, due to dysregulated Th17 activity and chronic inflammation ^[6-7]. Monoclonal antibodies targeting IL-23, such as risankizumab and guselkumab, selectively block the p19 subunit, demonstrating therapeutic efficacy in psoriasis and inflammatory bowel diseases by suppressing pathogenic IL-17/Th17 pathways ^[8]. While IL-23 plays a role in protective immunity, its overactivation contributes to tissue damage in autoimmune settings, highlighting its dual function in immune regulation and disease pathogenesis ^[6-9]. B6-hIL13/hIL23A mice are humanized models generated by crossing B6-hIL13 mice (Product No.: C001634) with B6-hIL23A mice (Product No.: C001618). These mice are suitable for studying the pathological mechanisms and therapeutic strategies of allergic and inflammatory diseases, immune-related disorders, and cancer, as well as for the screening, development, and preclinical evaluation of IL13/IL23A-targeted drugs.

The B6-huIL4/huIL13/huTSLP mouse is a triple-gene humanized model obtained by mating B6-huIL4 mice (catalog number: C001628), B6-huIL13 mice (catalog number: C001634), and B6-huTSLP mice (catalog number: C001809). This model can be used for the mechanism research and development of treatment methods in allergic diseases, inflammation and autoimmune diseases, Th2 immune response, parasitic infections, tumor immunology, as well as the development of IL-4/IL13/TSLP-targeted drugs, and the pre-clinical evaluation of drug efficacy and safety.