B6-IgG1 KO Mouse

Immunoglobulin G (IgG) is the most abundant type of immunoglobulin in human serum, accounting for about 75% of the total serum immunoglobulins. It also has the longest half-life among serum immunoglobulins. IgG is synthesized in the spleen and lymph nodes and is primarily distributed in serum and tissue fluids. It is a major component of antibodies against bacteria, toxins, and viruses, and plays a crucial role in the body's immune response against infections. IgG is the only immunoglobulin that can cross the placental barrier, playing an important role in neonatal infection protection ^[1]. There are four IgG subtypes in the human body, with the IgG1 subtype accounting for about 66% of the total serum IgG. IgG1 is very important for mediating antibody responses against viral pathogens. It can effectively bind to C1q, triggering complement-dependent cytotoxicity (CDC), and bind to various Fc receptors, inducing antibody-dependent cell-mediated cytotoxicity (ADCC). These are two of the most important functions in immune responses. Therefore, IgG1 has always been the preferred model for antibody therapy and is the most promising subtype in tumor immunotherapy ^[2-3].

Selective IgG Subclass Deficiency is one of the most common immunodeficiency diseases in children. Patients with this disease have reduced total serum IgG levels, or normal total IgG levels but one or more IgG subclasses below normal levels. In most cases, patients with IgG1 deficiency also have deficiencies in other IgG subclasses, often with low serum IgG levels. Those with deficiencies in other IgG categories are prone to developing common variable immunodeficiency (CVID). Patients usually have a lifelong history of susceptibility to pyogenic infections, which can develop into chronic, progressively worsening lung infections, and commonly have deficient antibody responses to diphtheria and tetanus toxins ^[4-5].

The mouse Ighg1 gene is homologous to the human IGHG1, IGHG2, and IGHG3 genes. B6-IgG1 KO mice are constructed by knocking out the Ighg1 gene in mice, creating a model of IgG1 deficiency. This model provides an effective tool for research on diseases related to IgG1 deficiency.