SOCS1 negatively regulates the production of Foxp3+ CD4+ T cells in the thymus

被引:23
作者
Zhan, Yifan [1 ]
Davey, Gayle M. [1 ]
Graham, Kate L. [2 ]
Kiu, Hiu [1 ]
Dudek, Nadine L. [3 ]
Kay, Thomas W. H. [2 ]
Lew, Andrew M. [1 ]
机构
[1] Royal Melbourne Hosp, Walter & Eliza Hall Inst Med Res, Parkville, Vic 3050, Australia
[2] St Vincents Inst, Fitzroy, Vic, Australia
[3] Univ Melbourne, Bio21 Inst, Parkville, Vic 3052, Australia
基金
英国医学研究理事会;
关键词
SOCS1; Foxp3; IFN-gamma; IL-7; VAV EXCHANGE FACTOR; CYTOKINE SIGNALING-1; LYMPHOCYTE DEVELOPMENT; DEFICIENT MICE; IN-VIVO; SUPPRESSOR; ACTIVATION; HOMEOSTASIS; PROTEINS; IL-7;
D O I
10.1038/icb.2009.23
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
SOCS1 profoundly influences the development and peripheral homeostasis of CD8(+) T cells but has less impact on CD4(+) T cells. Despite the moderate influence of SOCS1 in the development of the total CD4 T-cell lineage, we show here that SOCS1 deficiency resulted in a 10-fold increase in Foxp3(+) CD4(+) T cells in the thymus. Increased numbers of Foxp3(+) thymocytes occurred in mice with T-cell-specific ablation of SOCS1, suggesting that the effect is T-cell intrinsic. This increase in Foxp3(+) CD4(+) cells in SOCS1-deficient mice also occurred in the absence of IFN-gamma or/and IL-7 signaling. Increase in CD25(+)CD4(+) T cells in the absence of SOCS1 could be partly due to enhanced survival by CD25(+)CD4(+) cells, to a lesser degree CD25(-)CD4(+) T cells, from SOCS1-deficient mice with or without T-cell growth factors. Immunology and Cell Biology (2009) 87, 473-480; doi: 10.1038/icb.2009.23; published online 21 April 2009
引用
收藏
页码:473 / 480
页数:8
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