期刊
JOURNAL OF IMMUNOLOGY
卷 188, 期 7, 页码 3138-3149出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1101390
关键词
-
类别
资金
- Juvenile Diabetes Research Foundation [1-2005-903]
- Swedish Research Council [521-2009-5302]
- Swedish Diabetes Society
- Novo Nordisk Foundation
- Children's Diabetes Society in Sweden
- Wilhelm and Martina Lundgren Foundation
- Adlerbert Foundation
- Swedish Foundation for Strategic Research
Type 1 diabetes (T1D) is a chronic autoimmune disease that results from T cell-mediated destruction of pancreatic beta cells. CD1d-restricted NKT lymphocytes have the ability to regulate immunity, including autoimmunity. We previously demonstrated that CD1d-restricted type II NKT cells, which carry diverse TCRs, prevented T1D in the NOD mouse model for the human disease. In this study, we show that CD4(+) 24 alpha beta type II NKT cells, but not CD4/CD8 double-negative NKT cells, were sufficient to downregulate diabetogenic CD4(+) BDC2.5 NOD T cells in adoptive transfer experiments. CD4(+) 24 alpha beta NKT cells exhibited a memory phenotype including high ICOS expression, increased cytokine production, and limited display of NK cell markers, compared with double-negative 24 alpha beta NKT cells. Blocking of ICOS or the programmed death-1/programmed death ligand 1 pathway was shown to abolish the regulation that occurred in the pancreas draining lymph nodes. To our knowledge, these results provide for the first time cellular and molecular information on how type II CD1d-restricted NKT cells regulate T1D. The Journal of Immunology, 2012, 188: 3138-3149.
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