Intravenous immunoglobulin (
IVIg) has been shown to be effective for a variety of
autoimmune diseases. Despite its widespread use and therapeutic success, the precise mechanisms for the anti-inflammatory
therapeutic effects of
IVIg are not well understood. In particular, few reports have examined the mechanism of
IVIg on regulatory T cells (Treg: CD4(+)CD25(+)FoxP3(+) T cells). In the present study, to clarify the effect of intravenous
S-sulfonated immunoglobulin (S-
IVIg) on Treg, we investigated
experimental autoimmune encephalomyelitis (EAE), the representative animal model of
autoimmune disease. First, when we evaluated the effect of S-
IVIg in an acute EAE model, the prophylactic treatment of S-
IVIg dose-dependently controlled the symptoms of EAE. Next, we measured Treg in EAE mice spleen by flow cytometry. The percentage of Treg in S-
IVIg-treated mice was significantly increased compared with Saline-treated mice. Finally, in reinduced EAE, S-
IVIg not only prevented EAE progression, but also increased the percentage of Treg in the spleen. The increase in percentage of Treg in S-
IVIg-treated EAE might be associated with protection against EAE. These observations provide important evidence that
IVIg is effective in T-cell-mediated control of autoimmunity.