Many potential mechanisms of action for IVIG have been suggested [3] . Of them, at least three main mechanisms are suggested to explain the anti-inflammatory function of high dose IVIG: first, high-dose IgG saturates the neonatal FcRs (FcRn) and leads to the increased catabolism of autoantibodies; second, high-dose IgG saturates the activating Fcγ receptors (FcγRs) and prevents autoantibody-mediated activation of leukocytes; third, high-dose IgG increases the cell surface expression of inhibitory Fcγ receptors [4] . A single, N-linked glycosylation site exists at the amino acid 297 in the heavy chain of all IgG subclasses with approximately 10% terminating in sialic acid [5] . Recently, the α2, 6 sialylated IgG was reported to interact with a lectin receptor, specific 2