Gene interactions and pathways from curated databases and text-mining
J Immunol 2011, PMID: 21709159

The tuberous sclerosis complex-mammalian target of rapamycin pathway maintains the quiescence and survival of naive T cells.

Wu, Qi; Liu, Yu; Chen, Chong; Ikenoue, Tsuneo; Qiao, Yu; Li, Chi-Shan; Li, Weiquan; Guan, Kun-Liang; Liu, Yang; Zheng, Pan

Naive T cells receive stimulation from the positive selecting ligand in the periphery for their survival. This stimulation does not normally lead to overt activation of T cells, as the T cells remain largely quiescent until they receive either antigenic or lymphopenic stimuli. The underlying mechanism responsible for survival and quiescence of the naive T cells remains largely unknown. In this study, we report that T cell-specific deletion of Tsc1, a negative regulator of mammalian target of rapamycin, resulted in both spontaneous losses of quiescence and cellularity, especially within the CD8 subset. The Tsc1-deficient T cells have increased cell proliferation and apoptosis. Tsc1 deletion affects the survival and quiescence of T cells in the absence of antigenic stimulation. Loss of quiescence but not cellularity was inhibited by rapamycin. Our data demonstrate that tuberous sclerosis complex-mammalian target of rapamycin maintains quiescence and survival of T cells.

Diseases/Pathways annotated by Medline MESH: Lymphopenia
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Text Mining Data

mammalian target of rapamycin — Tsc1: " In this study, we report that T cell-specific deletion of Tsc1 , a negative regulator of mammalian target of rapamycin , resulted in both spontaneous losses of quiescence and cellularity, especially within the CD8 subset "

Manually curated Databases

No curated data.