How T lymphocytes switch between life and death

Rüdiger Arnold*, Dirk Brenner, Mareike Becker, Christian R. Frey, Peter H. Krammer

*Corresponding author for this work

Research output: Contribution to journalShort surveypeer-review

86 Citations (Scopus)


While insufficient cell death of activated T cells can result in autoimmune disorders, elimination of too many T cells can lead to immunodeficiency. Therefore, T lymphocyte fate is highly regulated and requires that cells can switch from an apoptosis-resistant towards an apoptosis-sensitive state. This switch is tightly controlled by various effector molecules. Basically, two separate pathways control the fate of antigen-activated T cells: activation-induced cell death (AICD) and activated T cell autonomous death (ACAD). Autoreactive T lymphocytes are eliminated by restimulation via their T cell receptor (TCR) and undergo AICD involving death receptors (extrinsic pathway). In contrast, ACAD can lead to T cell deletion without TCR restimulation, and is determined by the ratio between anti- and pro-apoptotic Bcl-2 family members at the mitochondria (intrinsic pathway). While the extrinsic and the intrinsic pathway lead to caspase activation, non-caspase proteases (e.g., cathepsins) can be released by the lysosomes and might contribute to AICD as well as to ACAD. Activated T cells posses cell death escape mechanisms which are needed for survival of (memory) T cells, but are deleterious for autoimmune disorders or progression of T cell lymphomas.

Original languageEnglish
Pages (from-to)1654-1658
Number of pages5
JournalEuropean Journal of Immunology
Issue number7
Publication statusPublished - Jul 2006
Externally publishedYes


  • AICD
  • CD95
  • Lysosomes
  • Mitochondria
  • TCR


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