mTORC2 in Thymic Epithelial Cells Controls Thymopoiesis and T Cell Development

被引:13
作者
Wang, Hong-Xia [1 ,2 ]
Cheng, Joyce S. [2 ,3 ]
Chu, Shuai [1 ,2 ]
Qiu, Yu-Rong [1 ]
Zhong, Xiao-Ping [2 ,4 ,5 ]
机构
[1] Southern Med Univ, Nanfang Hosp, Lab Med Ctr, Guangzhou 510515, Guangdong, Peoples R China
[2] Duke Univ, Med Ctr, Dept Pediat, Div Allergy & Immunol, Durham, NC 27710 USA
[3] Temple Univ, Premed BS MD Hlth Scholar Program, Philadelphia, PA 19222 USA
[4] Duke Univ, Med Ctr, Dept Immunol, Durham, NC 27710 USA
[5] Duke Univ, Med Ctr, Hematol Malignancies & Cellular Therapies Program, Duke Canc Inst, Durham, NC 27710 USA
基金
美国国家卫生研究院;
关键词
RAPAMYCIN COMPLEX 1; EFFECTOR FUNCTION; NEGATIVE SELECTION; MAMMALIAN TARGET; BETA-CATENIN; DIFFERENTIATION; LEUKEMIA; SELF; REPERTOIRE; ACTIVATION;
D O I
10.4049/jimmunol.1502698
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Thymic epithelial cells (TECs) play important roles in T cell generation. Mechanisms that control TEC development and function are still not well defined. The mammalian or mechanistic target of rapamycin complex (mTORC)2 signals to regulate cell survival, nutrient uptake, and metabolism. We report in the present study that mice with TEC-specific ablation of Rictor, a critical and unique adaptor molecule in mTORC2, display thymic atrophy, which accompanies decreased TEC numbers in the medulla. Moreover, generation of multiple T cell lineages, including conventional TCR alpha beta T cells, regulatory T cells, invariant NKT cells, and TCR gamma delta T cells, was reduced in TEC-specific Rictor-deficient mice. Our data demonstrate that mTORC2 in TECs is important for normal thymopoiesis and efficient T cell generation.
引用
收藏
页码:141 / 150
页数:10
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