期刊
JOURNAL OF AUTOIMMUNITY
卷 21, 期 3, 页码 221-237出版社
ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
DOI: 10.1016/S0896-8411(03)00114-8
关键词
CD4(+)CD25(+) regulatory T cells; insulin 13 : 9-23; non-obese diabetic mice; transforming growth factor-beta; type 1 diabetes
类别
NOD mice have a relative deficiency of CD4(+)CD25(+) regulatory T cells that could result in an inability to maintain peripheral tolerance. The aim of this study was to induce the generation of CD4(+)CD25(+) regulatory T cells in response to autoantigens to prevent type I diabetes (TlD). We found that immunization of NOD mice with insulin B-chain peptide 13:9-23 followed by 72 h in vitro culture with 13:9-23 peptide induces generation of CD4(+)CD25(+) regulatory T cells. Route of immunization has a critical role in the generation of these cells. Non-autoimmune mice BALB/c, C57BL/6 and NOR did not show up regulation of CD4(+)CD25(+) regulatory T cells. These cells secreted large amounts of TGF-beta and TNF-alpha with little or no IFN-gamma and IL-10. Adoptive transfer of these CD4(+)CD25(+) regulatory T cells into NOD-SCID mice completely prevented the adoptive transfer of disease by diabetogenic T cells. Although, non-self antigenic OVA (323-339) peptide immunization and in vitro culture with OVA (323-339) peptide does result in up regulation of CD4(+)CD25(+) T cells, these cells did not prevent transfer of diabetes. Our study for the first time identified the generation of antigen-specific CD4(+)CD25(+) regulatory T cells specifically in response to immunization with 13:9-23 peptide in NOD mice that are capable of blocking adoptive transfer of diabetes. Our results suggest the possibility of using autoantigens to induce antigen-specific regulatory T cells to prevent and regulate autoimmune diabetes. (C) 2003 Published by Elsevier Ltd.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据