Clinical Information

Produced during a secondary immune response, Immunoglobulin G (IgG) makes up the majority of immunoglobulin in the blood. During an infection, IgG molecules coat infecting microorganisms and bind to specific receptors on phagocytic cells such as macrophages and polymorphonuclear leukocytes. This helps facilitate phagocytosis. IgG can also activate the first component of the complement system, which unleashes a biochemical attack that kills the microorganism. IgG is also the predominate extravascular immunoglobulin where it neutralizes bacterial toxins and binds to microorganisms. IgG antibodies can bind to tumor cells to target them for destruction by killer cells that have IgG receptor sites. IgG molecules are the only antibodies that can cross the placenta. IgG provides a major line of defense against infection in the first weeks of life.

Deficiencies in IgG can be acquired or genetic. Thermal burns, pemphigus, nephrotic syndrome, protein-losing enteropathies, non-IgG myelomas or macroglobulinemia, pregnancy, Wiskott-Aldrich syndrome, myotonic dystrophy, anti-immunoglobulin antibodies, immunosuppressive therapy and non-IgG monoclonal gammopathies are all conditions associated with IgG deficiency.

Elevated IgG can be polyclonal, oligoclonal or monoclonal. Elevated polyclonal IgG levels are associated with autoimmune diseases (systemic lupus erythematosus, rheumatoid arthritis, Sjogren’s syndrome), sarcoidosis, chronic liver disease, some parasitic diseases, chronic or recurrent infections and intrauterine contraceptive devices. Malignancies, infections, some dysgammaglobulinemia, and autoimmune disorders are associated with elevated oligoclonal IgG. Lymphomas, leukemia, and IgG multiple myeloma are associated with elevated monoclonal IgG.

Quantification of IgG can be used to evaluate humoral immunity, establish diagnosis and monitor therapy. Reduction of IgG leads to susceptibility to infection from encapsulated bacteria.