Program death-1 regulates peripheral T cell tolerance via an anergy-independent mechanism

Copyright © 2012 Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 143(2012), 2 vom: 07. Mai, Seite 128-33
1. Verfasser: Qiao, Guilin (VerfasserIn)
Weitere Verfasser: Yang, Lifen, Li, Zhenping, Ying, Haiyan, Hassen, Yassir, Yin, Fei, Zhang, Jian
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2012
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Homeodomain Proteins Pdcd1 protein, mouse Programmed Cell Death 1 Receptor RAG-1 protein 128559-51-3
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520 |a Program death-1 (PD-1) has been documented to negatively regulate immune responses. However, the cellular and molecular mechanisms for PD-1-mediated immune suppression have not been fully elucidated. In this study, we show that loss of PD-1 does not lead to defective induction of CD4(+) T cell anergy in vitro and in vivo. Rather, the absence of PD-1 inhibits the development of inducible CD4(+)Foxp3(+) regulatory T cells (iTregs) induced by TGF-β in vitro. In support of this finding, PD-1 deficiency impairs the generation of iTregs in vivo and leads to development of severe T cell-transfer-induced colitis. Mechanistically, defective iTreg generation in the absence of PD-1 was attributed to the heightened phosphorylation of Akt. Therefore, we first demonstrate that PD-1 controls peripheral T cell tolerance via an anergy-independent but iTreg-dependent mechanism 
650 4 |a Journal Article 
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650 4 |a Research Support, Non-U.S. Gov't 
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700 1 |a Yang, Lifen  |e verfasserin  |4 aut 
700 1 |a Li, Zhenping  |e verfasserin  |4 aut 
700 1 |a Ying, Haiyan  |e verfasserin  |4 aut 
700 1 |a Hassen, Yassir  |e verfasserin  |4 aut 
700 1 |a Yin, Fei  |e verfasserin  |4 aut 
700 1 |a Zhang, Jian  |e verfasserin  |4 aut 
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