Enhancement of Regulatory T Cell Induction by Intravenous S-sulfonated Immunoglobulin during the Treatment of Experimental Autoimmune Encephalomyelitis
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- Okuda Sachio
- The Chemo-Sero-Therapeutic Research Institute (KAKETSUKEN)
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- Kamei Shintaro
- The Chemo-Sero-Therapeutic Research Institute (KAKETSUKEN)
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- Harano Satomi
- The Chemo-Sero-Therapeutic Research Institute (KAKETSUKEN)
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- Shinya Noriko
- The Chemo-Sero-Therapeutic Research Institute (KAKETSUKEN)
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- Hayashida Kenshi
- The Chemo-Sero-Therapeutic Research Institute (KAKETSUKEN)
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- Sasaki Takumi
- The Chemo-Sero-Therapeutic Research Institute (KAKETSUKEN)
Bibliographic Information
- Other Title
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- 実験的自己免疫性脳脊髄炎の治療における静注用スルホ化免疫グロブリンによる制御性T細胞の誘導
- ジッケンテキ ジコ メンエキセイ ノウ セキズイエン ノ チリョウ ニ オケル ジョウチュウヨウ スルホカ メンエキ グロブリン ニ ヨル セイギョセイ T サイボウ ノ ユウドウ
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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.<br>
Journal
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- YAKUGAKU ZASSHI
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YAKUGAKU ZASSHI 132 (2), 243-249, 2012-02-01
The Pharmaceutical Society of Japan
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Details 詳細情報について
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- CRID
- 1390001206127347328
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- NII Article ID
- 130001872016
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- NII Book ID
- AN00284903
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- ISSN
- 13475231
- 00316903
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- NDL BIB ID
- 023511193
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- Text Lang
- ja
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- Data Source
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- JaLC
- NDL
- Crossref
- CiNii Articles
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- Abstract License Flag
- Disallowed