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Autophagy is essential for effector CD8 + T cell survival and memory formation

  • Xiaojin Xu
  • , Koichi Araki
  • , Shuzhao Li
  • , Jin Hwan Han
  • , Lilin Ye
  • , Wendy G. Tan
  • , Bogumila T. Konieczny
  • , Monique W. Bruinsma
  • , Jennifer Martinez
  • , Erika L. Pearce
  • , Douglas R. Green
  • , Dean P. Jones
  • , Herbert W. Virgin
  • , Rafi Ahmed

Research output: Contribution to journalArticlepeer-review

Abstract

The importance of autophagy in the generation of memory CD8 + T cells in vivo is not well defined. We report here that autophagy was dynamically regulated in virus-specific CD8 + T cells during acute infection of mice with lymphocytic choriomeningitis virus. In contrast to the current paradigm, autophagy decreased in activated proliferating effector CD8 + T cells and was then upregulated when the cells stopped dividing just before the contraction phase. Consistent with those findings, deletion of the gene encoding either of the autophagy-related molecules Atg5 or Atg7 had little to no effect on the proliferation and function of effector cells, but these autophagy-deficient effector cells had survival defects that resulted in compromised formation of memory T cells. Our studies define when autophagy is needed during effector and memory differentiation and warrant reexamination of the relationship between T cell activation and autophagy.

Original languageEnglish
Pages (from-to)1152-1161
Number of pages10
JournalNature immunology
Volume15
Issue number12
DOIs
StatePublished - Nov 18 2014

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