How Privigen IVIg therapy works to treat PI, CIDP, and chronic ITP

Intravenous immunoglobulin (IVIg) therapy involves modulation of the expression and function of Fc receptors, interference with the activation of the complement system and cytokine network, regulation of cell growth, and other significant processes. These intricate effects underscore how important immunoglobulins are in the immune homeostasis of healthy individuals.^22,23

Two widely studied and accepted mechanisms of IVIg action are:

Supplementation of essential antibodies^22,23
Immunomodulatory effects^22,23

Choose a condition below to learn more about how Privigen works specifically in that disorder.

PI

CIDP

Chronic ITP

The mechanism of action of IgG in primary immunodeficiency (PI) disease has not been fully elucidated. It is known that Privigen provides patients with a broad spectrum of opsonic and neutralizing IgG antibodies against bacterial, viral, parasitic, and mycoplasma agents and their toxins.

Privigen is manufactured from the plasma of a large pool of healthy blood donors and therefore includes a broad variety of antibody specificities against common pathogens to which the donor population has been exposed²²
The antibodies in Privigen are structurally and functionally intact, and their effector functions are fully operative¹⁸

The mechanism of action for IgG therapy is complex and not fully understood. However, its success in treating CIDP—an inflammatory neuropathy with an underlying autoimmune basis—is largely attributed to its immunomodulatory effects.²⁴

A more precise mechanism of action regarding just how IgG therapy exerts its immunomodulatory effects is still being explored, but proposed mechanisms that may play a role include²⁴:

Reducing T-cell activity potentially involved in the development of CIDP
Mediating Fc receptor blockade on macrophages, which may inhibit demyelination
Modulating cell migration, which may prevent autoimmune complications
Neutralizing superantigens that may be involved in relapses caused by infection

The mechanism of action of IgG in chronic immune thrombocytopenic purpura (ITP) is complex and not fully understood. However, the success of treating chronic ITP with IgG has been attributed to the competitive inhibition of Fc receptors on phagocytic cells.^23,25

Continuing research indicates that other mechanisms may also contribute to thrombocytopenia, including²²:

Induction of Fcγ IIb inhibitory receptors, which appear to play a critical role in thrombocytopenia
Regulatory properties of anti-idiotypic antibodies, which possibly regulate the immune system
Long-term effects of downregulation on autoantibodies

Although IVIg has been used to treat chronic ITP, the mechanism of action is still unclear. Further research will be needed to better understand how IVIg works in chronic ITP.²²

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