Intravenous Immunoglobulins: Mode of Action and Indications in Autoimmune and Inflammatory Dermatoses

Table 1

Mechanism of action of IVIG in inflammatory and autoimmune dermatoses.

Biologic target	Mode of action	Reference
T-lymphocytes	Inhibition of T cell derived IL-2, IL-10, TNF-β, and IFN-γ; Antibodies against CD4 cells, HLA class I and II molecules, and T cell receptor β chain	[2–4]
B-lymphocytes	Antibody neutralization and inhibition of Ab production due B-lymphocytes binding; Inhibition of IL-6 and TNF-α production; Induction of B-cell apoptosis	[5–7]
Monocyte/macrophage system	Suppressing the phagocytosis of antibody-coated cells by Fc blockade; Anti-inflammatory activity of IVIG through the surface expression of inhibitory Fc γRIIB receptor; IVIG increasing the synthesis of IL-8 in cultures of monocytes	[8]; [9]; [2, 10]
Dendritic cells	Suppression of the dendritic cells differentiation maturation and capacity to secrete IL-12 on activation	[11, 12]
Keratinocytes	Blockage of Fas-mediated keratinocyte death by binding to the CD95 (death receptor)	[13, 14]
Complement system	IVIG having immediate and long-lasting attenuating effect on complement amplification in vivo by stimulating inactivation of C3 convertase precursors	[15]; [16]