IgGTransport

IgGTransport refers to the movement of immunoglobulin G (IgG) across cellular barriers, enabling distribution, immune surveillance, and the maintenance of serum IgG levels. The central mechanism is neonatal Fc receptor (FcRn)–mediated transcytosis. IgG binds FcRn in acidic endosomes after cellular uptake; FcRn protects IgG from lysosomal degradation and releases it at the neutral pH of the blood or basolateral surfaces. This recycling process extends IgG’s half-life and allows selective trafficking between compartments, contributing to the steady-state concentration of IgG in circulation and tissues.

In physiological contexts, FcRn-driven transport is critical for maternal to fetal IgG transfer in pregnancy. FcRn expressed in placental syncytiotrophoblasts mediates the selective passage of maternal IgG into the fetal circulation, with transfer increasing in later gestation and favoring certain IgG subclasses. Subclass differences exist, with IgG1 and IgG3 typically transported more efficiently than IgG2, and IgG4 at intermediate levels. FcRn also participates in IgG movement across other epithelial and endothelial barriers, including mucosal surfaces and the brain’s microvasculature, though the extent of transport varies by tissue, receptor expression, and local pH.

Clinically, IgGTransport influences the pharmacokinetics of therapeutic antibodies and intravenous immunoglobulin (IVIG). Modulating FcRn activity can alter circulating IgG levels, providing a strategy to reduce pathogenic antibodies in autoimmune diseases. FcRn inhibitors are under development or in use for such indications. Variations in IgGTransport can affect immune protection, vaccine responses, and the efficacy of antibody-based therapies, making FcRn a focal point in immunology and therapeutic design.