期刊
JOURNAL OF IMMUNOLOGY
卷 182, 期 8, 页码 4516-4520出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0803161
关键词
-
类别
资金
- NIAID NIH HHS [R01 AI050761-07A1, R01 AI054912, R01 AI050761-06, R01 AI054912-02, AI054912, R01 AI050761, R01 AI054912-03] Funding Source: Medline
T cell activation and tolerance are delicately regulated by costimulatory molecules. Although B and T lymphocyte attenuator (BTLA) has been shown as a negative regulator for T cell activation, its role in peripheral T cell tolerance induction in vivo has not been addressed. In this study, we generated a novel strain of BTLA-deficient mice and used three different models to characterize the function of BTLA in controlling T cell tolerance. In an oral tolerance model, BTLA-deficient mice were found resistant to the induction of T cell tolerance to an oral Ag. Moreover, compared with wild-type OT-II cells, BTLA(-/-) OT-II cells were less susceptible to tolerance induction by a high-dose OVA peptide administered i.v. Finally, BTIA(-/-) OT-I cells caused autoimmune diabetes in RIP-mOVA recipient mice. Our results thus demonstrate an important role for BTLA in the induction of peripheral tolerance of both CD4(+) and CD8(+) T cells in vivo. The Journal of Immunology, 2009, 182: 4516-4520.
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