Abstract
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.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
