Immunological unresponsiveness characterized by increased expression of CD5 on peripheral T cells induced by dentritic cells in vivo

被引:178
作者
Hawiger, D
Masilamani, RF
Bettelli, E
Kuchroo, VK
Nussenzweig, MC
机构
[1] Rockefeller Univ, Lab Mol Immunol, New York, NY 10021 USA
[2] Howard Hughes Med Inst, New York, NY 10021 USA
[3] Brigham & Womens Hosp, Ctr Neurol Dis, Boston, MA 02115 USA
[4] Harvard Univ, Sch Med, Boston, MA 02115 USA
基金
美国国家卫生研究院;
关键词
D O I
10.1016/j.immuni.2004.05.002
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
In the steady state, interaction between T cells and antigen-presenting dendritic cells (DCs) leads to T cell tolerance. To examine the role of DC regulated peripheral tolerance in a model autoimmune disease, we delivered an encephalitogenic oligodendrocyte glycoprotein (MOG) peptide to DCs in vivo. We found that targeting MOG peptide to DCs resulted in a novel form of peripheral T cell tolerance that was sufficiently profound to prevent autoimmune experimental acute encephalomyelitis (EAE). The tolerized T cells were severely impaired in specific secondary responses to antigen in vivo but they were not intrinsically anergic since they remained highly responsive to T cell receptor (TCR) stimulation in vitro. The mechanism that mediates this dynamic antigen-specific T cell unresponsiveness differs from previously described forms of tolerance in that it requires that DCs induce CD5 expression on activated T cells.
引用
收藏
页码:695 / 705
页数:11
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