Many improvements have been made in our knowledge of the processes through which intravenous immune globulin (IVIG) regulates immune activity in autoimmune diseases in recent years. Previous research has focused on the Fc domain of the IgG molecule, as well as the involvement of the FcRIIB receptor and the sialylated Fc domain in mediating anti-inflammatory effects in mouse models of autoantibody-mediated illnesses. Recent research has linked the F(ab’)2 domain to IVIG-induced immune modulation in T-cell-mediated autoimmune disease models, with activation of T-regulatory cells and downregulation of the Th17 pathways being essential components of this process. The prostaglandin E route may be involved in the alterations in the T-regulatory pathway caused by IVIG.
Many of the hypothesized pathways for IVIG’s immune-modulating actions highlight the complexities of immune effector activities in disease processes. Although there is debate over the involvement of the FcRIIB receptor and the significance of the sialylated Fc domain in human autoimmune illnesses, it is likely that no one mechanism is responsible for the effects of IVIG in autoimmune and inflammatory diseases. The possible participation of the prostaglandin E pathway might lead to new therapies.
