Autoimmunity occurs when the immune system mistakenly attacks the body’s own healthy tissues, leading to chronic inflammation and damage. This immune overactivity can paradoxically lead to a deficiency in protective components. Immunoglobulin G (IgG) is the most abundant type of antibody, representing the primary line of defense responsible for long-term protection against pathogens. A low level of IgG, known as hypogammaglobulinemia, creates a vulnerability that significantly compromises health.
The Role of Immunoglobulin G
IgG is the main antibody found in blood and extracellular fluid, making up approximately 75% of the total immunoglobulins in the serum. It is produced by specialized white blood cells called plasma cells following an immune response. This antibody is responsible for memory immunity, ensuring a rapid defense upon re-exposure to a familiar threat.
IgG defends the body through several specific actions. Neutralization involves binding directly to toxins or viruses to prevent them from entering cells. It also uses opsonization, coating a pathogen to mark it for destruction by phagocytic immune cells. Uniquely, IgG is the only antibody class capable of crossing the placenta, providing newborns with temporary passive immunity.
Autoimmune Diseases Associated with Low IgG
The decrease in IgG is most often a secondary complication resulting from the underlying autoimmune disease or its required treatments. One well-documented condition is Systemic Lupus Erythematosus (SLE), which affects multiple organs and involves immune cell dysregulation. Patients with severe Rheumatoid Arthritis (RA) can also develop low IgG levels, particularly when the disease is highly active.
Sjögren’s Syndrome, which primarily targets moisture-producing glands, is another systemic autoimmune condition where hypogammaglobulinemia can occur. Localized autoimmune conditions affecting the digestive tract, such as Celiac disease or severe Autoimmune Enteropathy, are also known to lead to reduced antibody levels. This reduction in protective antibodies often complicates the patient’s clinical course by increasing susceptibility to bacterial infections.
Why Autoimmunity Causes Reduced IgG Levels
The mechanisms leading to reduced IgG are generally divided into issues of production and loss. A significant factor is the use of immunosuppressive medications necessary to control autoimmune disease activity. Drugs that target B cells, such as rituximab, actively deplete the cells responsible for producing all immunoglobulins, leading to a profound reduction in antibody levels.
Other common treatments, including corticosteroids and various chemotherapy agents, can suppress the function of the bone marrow and B cells, limiting antibody production. Furthermore, the chronic, widespread inflammation characteristic of many autoimmune diseases can accelerate the breakdown, or catabolism, of existing IgG antibodies. This increased destruction depletes the body’s reserves faster than they can be replenished.
In some autoimmune gastrointestinal disorders, such as protein-losing enteropathy, the inflamed gut lining becomes leaky. This allows serum proteins, including IgG antibodies, to escape into the digestive tract and be lost from the body. Consequently, the combination of reduced production and increased loss contributes to the low IgG state seen in these autoimmune contexts.
Managing Secondary Immunodeficiency
A lowered IgG level places the patient at a significantly higher risk for recurrent bacterial infections, particularly those affecting the respiratory system, such as pneumonia and chronic sinusitis. Management of this secondary immunodeficiency begins with careful monitoring of serum IgG levels and assessing the patient’s ability to produce specific antibodies following vaccination. Preventative measures, including appropriate vaccinations and prophylactic antibiotics, are often employed to mitigate the infection risk.
For patients with critically low IgG levels who experience frequent or severe infections, Immunoglobulin Replacement Therapy (IRT) may be necessary. This treatment involves infusing concentrated IgG antibodies pooled from healthy donors, administered intravenously (IVIG) or subcutaneously (SCIG). IRT supplements the body’s deficient antibody pool, providing immediate passive immunity to fight off pathogens. Patients dealing with this complex intersection should seek guidance from specialists, such as an immunologist or rheumatologist, to tailor a specific management plan.