Effect of inhibiting the signal of mammalian target of rapamycin on memory T cells.

Abstract Background Mammalian target of rapamycin (mTOR) signaling is crucial to the activation and proliferation of T cells. Memory T cells can significantly hinder the induction of transplant tolerance. Resent research demonstrates that mTOR signaling regulates the survival and function of memory T cells. Materials and Methods Naive T cells were adoptively transferred to Rag −/− mice to generate similar memory T cells that undergo homeostatic proliferation. These memory T cells were then used to examine the effect of mTOR inhibition on the function of memory T cells. The effect of inhibiting mTOR signaling on the apoptosis of memory T cells was also examined. Results Quantitative reverse-transcription polymerase chain reaction analysis showed that the expression of mTOR signaling was substantially lower in memory T cells. The levels of interferon-γ, interleukin (IL)-2, IL-4, and IL-10 decreased after mTOR inhibition; the expression of Bcl-2 increased in memory CD8 + T cells and decreased in memory CD4 + T cells; and Bax increased in memory CD4 + T cells and decreased in memory CD8 + T cells. Memory CD4 + T cells were more sensitive to apoptotic cell death in this model after mTOR inhibition. Memory CD8 + T cells were not affected by mTOR inhibition. Conclusions mTOR was crucial to homeostatic proliferation-induced memory T cells. The critical mechanisms of mTOR signaling inhibition are suppressed the functions of memory T cells and promoted the apoptosis of memory CD4 + T cells.