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B6-Igha KO Mouse
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B6-Igha KO Mouse
製品名
B6-Igha KO Mouse
製品ID
C001394
系統名
C57BL/6JCya-Ighaem1/Cya
背景情報
C57BL/6JCya
状況
このマウス系統を論文で使用する場合は、「B6-Igha KO Mouse(カタログ番号C001394)はサイアジェンから購入しました。」と引用してください。
Other Immunodeficient Mice
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
Other Immunodeficient Mice
基本情報
検証 Data
関連リソース
基本情報
系統詳細
Immunoglobulin A (IgA) is the second most abundant immunoglobulin in serum, comprising 10–20% of serum immunoglobulins, following IgG. IgA is primarily produced by the mucosal tissues of the digestive, respiratory, and urogenital systems, where mucosal-associated lymphoid tissues generate IgA to counteract pathogen invasion. Additionally, IgA is present in saliva, tears, and breast milk [1]. In the human body, IgA can be classified into serum IgA and secretory IgA based on its location. Serum IgA exhibits relatively weak immune functions [2], whereas secretory IgA is a critical component of the mucosal defense system. It is widely distributed in breast milk, saliva, and mucosal secretions of the gastrointestinal, respiratory, and urogenital tracts, playing an essential role in inhibiting microbial adhesion to respiratory epithelium and reducing viral replication. IgA possesses antibody activity against certain viruses, bacteria, and general antigens, serving as the first line of defense against pathogen invasion [3].
Selective immunoglobulin A (IgA) deficiency is a systemic immunological disorder caused by a primary immunodeficiency characterized by the absence of detectable IgA in the blood and secretions, while other immunoglobulin types remain unaffected. The function of T lymphocytes, phagocytes, and the complement system in these patients is also preserved. Approximately half of the patients with selective IgA deficiency are susceptible to recurrent infections, such as otitis media, sinusitis, bronchitis, and pneumonia [4]. Moreover, these patients exhibit a significantly increased prevalence of autoimmune diseases, including rheumatoid arthritis, systemic lupus erythematosus, and immune thrombocytopenic purpura, as well as allergic conditions such as asthma [4-5].
The B6-IgA KO mouse is an IgA-deficient model developed by knocking out the mouse Igha gene, which encodes IgA, in mice. This mouse model provides a valuable tool for studying diseases associated with selective IgA deficiency.
参考文献
Pabst O. New concepts in the generation and functions of IgA. Nat Rev Immunol. 2012 Dec;12(12):821-32.
de Fays C, Carlier FM, Gohy S, Pilette C. Secretory Immunoglobulin A Immunity in Chronic Obstructive Respiratory Diseases. Cells. 2022 Apr 13;11(8):1324.
Corthésy B. Role of secretory immunoglobulin A and secretory component in the protection of mucosal surfaces. Future Microbiol. 2010 May;5(5):817-29.
Yazdani R, Azizi G, Abolhassani H, Aghamohammadi A. Selective IgA Deficiency: Epidemiology, Pathogenesis, Clinical Phenotype, Diagnosis, Prognosis and Management. Scand J Immunol. 2017 Jan;85(1):3-12.
Hiemstra PS. Immunoglobulin A in asthma: friend or foe? Eur Respir J. 1998 Sep;12(3):517-8.
系統作製戦略
The Igha gene is located on chromosome 12 in mice, and exons 1~4 were knocked out using gene editing technology.

Figure 1. Diagram of the gene editing strategy for the generation of B6-Igha KO mice.
適用分野
Study of selective immunoglobulin A (IgA) deficiency;
Research on autoimmune and allergic diseases related to IgA deficiency;
Investigation of the mechanisms and functions of immunoglobulin A (IgA).
検証 Data
関連リソース
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