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huIL4(BALB/c) Mouse
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huIL4(BALB/c) Mouse
製品名
huIL4(BALB/c) Mouse
製品ID
C001780
系統名
BALB/cAnCya-Il4em1(hIL4)/Cya
背景情報
BALB/cAnCya
状況
このマウス系統を論文で使用する場合は、「huIL4(BALB/c) Mouse(カタログ番号C001780)はサイアジェンから購入しました。」と引用してください。
HUGO-GT Humanized Models
Immune Target Humanized Mouse Models
Cytokine Gene Humanized Mouse Models
製品タイプ
年齢
遺伝子型
性別
数量
標準的な配送方法では、少なくとも3匹のヘテロ接合体キャリアを保証しています。ホモ接合体キャリアや指定された性別の個体の繁殖サービスも利用可能です。
お見積もりについてはこちらまでご連絡ください
HUGO-GT Humanized Models
Immune Target Humanized Mouse Models
Cytokine Gene Humanized Mouse Models
基本情報
検証 Data
関連リソース
基本情報
遺伝子名
遺伝子別名
BSF1, IL-4, BCGF1, BSF-1, BCGF-1
NCBI ID
染色体
Chr 5
MGI ID
さらに
系統詳細
Interleukin-4 (IL-4) and its receptor, IL-4R, are pivotal regulators of immune responses and inflammation. The IL4 gene encodes the IL-4 cytokine, a multifunctional protein predominantly secreted by Th2 cells, mast cells, and eosinophils, while the IL4R gene encodes the IL-4 receptor, which is expressed on a variety of immune cells, including B cells, T cells, macrophages, and endothelial cells. IL-4 binds to IL-4R, which exists in two distinct forms: Type I (comprising IL-4Rα and the common γ-chain) and Type II (comprising IL-4Rα and IL-13Rα1) [1]. This interaction activates the JAK-STAT signaling pathway, driving Th2 cell differentiation, B cell class switching to IgE, and anti-inflammatory responses. The IL-4/IL-4R signaling axis is critically implicated in allergic diseases such as asthma, atopic dermatitis, and allergic rhinitis, as well as in parasitic infections and certain cancers [2-5]. Dysregulation of this pathway underlies various pathological conditions, positioning IL-4 as a promising therapeutic target.
The huIL4(BALB/c) mouse is a humanized model constructed via gene-editing technology, where the sequences from the start codon to the stop codon of the endogenous mouse Il4 gene were replaced with those of the human IL4 gene. This model serves as a valuable tool for researching allergic diseases (such as asthma and atopic dermatitis), Th2 immune responses, parasitic infections, tumor immunology, and chronic inflammation. Additionally, it provides a robust preclinical research platform for evaluating the efficacy and mechanisms of therapeutic drugs targeting the IL-4 pathway.
参考文献
Gandhi NA, Bennett BL, Graham NM, Pirozzi G, Stahl N, Yancopoulos GD. Targeting key proximal drivers of type 2 inflammation in disease. Nat Rev Drug Discov. 2016 Jan;15(1):35-50.
Oetjen LK, Mack MR, Feng J, Whelan TM, Niu H, Guo CJ, Chen S, Trier AM, Xu AZ, Tripathi SV, Luo J, Gao X, Yang L, Hamilton SL, Wang PL, Brestoff JR, Council ML, Brasington R, Schaffer A, Brombacher F, Hsieh CS, Gereau RW 4th, Miller MJ, Chen ZF, Hu H, Davidson S, Liu Q, Kim BS. Sensory Neurons Co-opt Classical Immune Signaling Pathways to Mediate Chronic Itch. Cell. 2017 Sep 21;171(1):217-228.e13.
Bankaitis KV, Fingleton B. Targeting IL4/IL4R for the treatment of epithelial cancer metastasis. Clin Exp Metastasis. 2015 Dec;32(8):847-56.
Davoodi P, Mahesh PA, Holla AD, Ramachandra NB. A preliminary study on the association of single nucleotide polymorphisms of interleukin 4 (IL4), IL13, IL4 receptor alpha (IL4Rα) & Toll-like receptor 4 (TLR4) genes with asthma in Indian adults. Indian J Med Res. 2015 Dec;142(6):675-80.
Choy DF, Hart KM, Borthwick LA, Shikotra A, Nagarkar DR, Siddiqui S, Jia G, Ohri CM, Doran E, Vannella KM, Butler CA, Hargadon B, Sciurba JC, Gieseck RL, Thompson RW, White S, Abbas AR, Jackman J, Wu LC, Egen JG, Heaney LG, Ramalingam TR, Arron JR, Wynn TA, Bradding P. TH2 and TH17 inflammatory pathways are reciprocally regulated in asthma. Sci Transl Med. 2015 Aug 19;7(301):301ra129.
系統作製戦略
The sequences from the start codon to the stop codon of the endogenous mouse Il4 gene were replaced with the sequences from the start codon to the stop codon of the human IL4 gene.

Figure 1. Gene editing strategy of huIL4(BALB/c) mice.
適用分野
Investigation of immune regulation and Th2 responses, allergic diseases, parasitic infections, and tumor immunology;
Preclinical development, screening, and efficacy evaluation of IL4-targeted therapeutic agents;
Studies on inflammation and autoimmune diseases.
検証 Data
1. Gene Expression (RT-qPCR)
Human IL4 and mouse Il4 transcript levels were analyzed by RT-qPCR in the spleen, thymus, and lung tissues of huIL4(BALB/c) and wild-type (WT) mice using human- and mouse-specific primers, respectively. Mouse Gapdh (mGapdh) was used as the endogenous control, and the relative transcript level of each gene was calculated for each tissue. Data are presented as mean±SD. Human IL4 transcripts were detected in the spleen, thymus, and lung tissues of huIL4(BALB/c) mice, whereas mouse Il4 transcripts were not detected. In contrast, mouse Il4 transcripts were detected in the corresponding tissues of WT mice, whereas human IL4 transcripts were not detected.

Figure 2. RT-qPCR analysis of human IL4 and mouse Il4 transcript levels in the spleen, thymus, and lung tissues of huIL4(BALB/c) and wild-type (WT) mice (6-week-old, female, homozygous, n=4).
2. Protein Expression (ELISA)
Serum was harvested from huIL4(BALB/c) and wild-type (WT) mice 3 hours after stimulation via intraperitoneal (i.p.) injection of anti-CD3ε (7.5 μg/mouse), and the expression levels of human IL-4 and mouse Il-4 were determined by ELISA. Data are presented as mean±SD. The results showed that human IL-4 protein was detected in the serum of huIL4(BALB/c) mice, while human IL-4 protein was not detected in WT mice. In contrast, mouse Il-4 protein was detected in the serum of WT mice, while mouse Il-4 protein was not detected in huIL4(BALB/c) mice.

Figure 3. The expression levels of human IL-4 and mouse Il-4 proteins in the serum of huIL4(BALB/c) mice and wild-type (WT) mice were detected by ELISA (7–8 weeks old, female, homozygous, n=5).
関連リソース
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