Intravenous immunoglobulin (IVIg) has been used for many years in the treat
ment of primary and secondary antibody deficiencies. IVIg was first demonst
rated to be effective in autoimmune desorders twenty years ago in the treat
ment of idiopathic thrombocytopenic purpura. The beneficial effect of IVIg
has since been established in the Guillain-Barre syndrome, chronic inflamma
tory demenilating polyneuropathy, myasthenia gravis, dermatomyositis, Kawas
aki syndrome and graft versus host disease. The beneficial effect of IVIg h
as been suggested in a large number of other auto-immune and systemic infla
mmatory conditions. The mode of action of IVIg is complex, involving Fc rec
eptor blockade, interference with complement activation and the cytokine ne
twork, provision of anti-idiotypic antibodies and modulation of T and B cel
l activation and differentiation. Such a broad range of activities reflects
the function of normal circulating immunoglobulins in maintaining toleranc
e to self in healthy individuals.