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.