title: 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.
  
  
  METHODS
  Naïve 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.
authors.affiliation: Medical School of Southeast University, Department of Urology, Affiliated Zhongda Hospital of Southeast University, Nan Jing, China.
authors.forename: S
authors.initials: S
authors.lastname: Chen
authors.affiliation: Medical School of Southeast University, Department of Urology, Affiliated Zhongda Hospital of Southeast University, Nan Jing, China.
authors.forename: D
authors.initials: D
authors.lastname: Liu
authors.affiliation: Department of Urology, Affiliated Nanjing First Hospital, Nanjing Medical University, Nan Jing, China.
authors.forename: J
authors.initials: J
authors.lastname: Wu
authors.affiliation: Medical School of Southeast University, Department of Urology, Affiliated Zhongda Hospital of Southeast University, Nan Jing, China.
authors.forename: B
authors.initials: B
authors.lastname: Xu
authors.affiliation: Medical School of Southeast University, Department of Urology, Affiliated Zhongda Hospital of Southeast University, Nan Jing, China.
authors.forename: K
authors.initials: K
authors.lastname: Lu
authors.affiliation: Medical School of Southeast University, Department of Urology, Affiliated Zhongda Hospital of Southeast University, Nan Jing, China.
authors.forename: W
authors.initials: W
authors.lastname: Zhu
authors.affiliation: Medical School of Southeast University, Department of Urology, Affiliated Zhongda Hospital of Southeast University, Nan Jing, China. Electronic address: mingchen6308@163.com.
authors.forename: M
authors.initials: M
authors.lastname: Chen
mesh_terms: D000818:Animals; D001483:Base Sequence; D017931:DNA Primers; D005434:Flow Cytometry; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction; D058570:TOR Serine-Threonine Kinases / Q000037:antagonists & inhibitors* / Q000378:metabolism
chemical_list: D017931:DNA Primers; C546843:mTOR protein, mouse; D058570:TOR Serine-Threonine Kinases