Wu, Q., Liu, Y., Chen, C., Ikenoue, T., Qiao, Y., Li, C. S., Li, W. Q., Guan, K. L., Zheng, P. (August 2011) The Tuberous Sclerosis Complex-Mammalian Target of Rapamycin Pathway Maintains the Quiescence and Survival of Naive T Cells. Journal of Immunology, 187 (3). pp. 1106-1112. ISSN 0022-1767
Abstract
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.
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