期刊
SEMINARS IN IMMUNOLOGY
卷 18, 期 2, 页码 89-92出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.smim.2006.01.011
关键词
Treg; Foxp3; Treg conversion; autoimmunity; diabetes; tumor immunity
类别
资金
- NIAID NIH HHS [R37AI53102] Funding Source: Medline
In order to exploit regulatory T cells in a clinical setting it is desirable to be able to generate such cells by a variety of antigens that elicit unwanted immune responses. This goal has been achieved by targeting antigen to dendritic cells under subimmunogenic conditions which results in the conversion of naive Foxp3 negative T cells into Foxp3-expressing regulatory T cells that are indistinguishable from what has been referred to as natural Treg. Such cells have the ability to interfere with immunity at early as well as late stages of the immune response during which effector cells have already been formed. This suggests that Treg cannot only be exploited to prevent immune responses but also to interfere with already established immunity. (c) 2006 Elsevier Ltd. All rights reserved.
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