T-lymphocyte death during shutdown of an immune response

Trends Immunol. 2004 Nov;25(11):610-5. doi: 10.1016/j.it.2004.08.012.

Abstract

The immune system serves to protect organisms from infectious pathogens. During infection, lymphocytes and cells of the innate immune system, expressing receptors that recognize foreign antigens, proliferate and differentiate to develop effector functions that help to kill the pathogens. Effector functions, such as cellular or antibody mediated cytotoxicity, and inflammatory cytokines can be harmful to the host. To limit damage to healthy tissue, mechanisms have evolved to shut down immune responses, including cell inactivation and cell death. Here we discuss recent studies demonstrating that the death of antigen-activated T lymphocytes during termination of an immune response is initiated by the BH3-only Bcl-2 family member Bim and also requires its multi-BH domain pro-apoptotic relatives Bax and Bak.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis / immunology*
  • Apoptosis Regulatory Proteins
  • Bcl-2-Like Protein 11
  • Carrier Proteins / metabolism
  • Humans
  • Membrane Proteins / metabolism
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Signal Transduction
  • T-Lymphocytes / cytology*
  • T-Lymphocytes / immunology*
  • T-Lymphocytes / metabolism
  • fas Receptor / metabolism

Substances

  • Apoptosis Regulatory Proteins
  • BCL2L11 protein, human
  • Bcl-2-Like Protein 11
  • Carrier Proteins
  • Membrane Proteins
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • fas Receptor