What do we know about the mechanisms of elimination of autoreactive T and B cells and what challenges remain

Immunol Cell Biol. 2008 Jan;86(1):57-66. doi: 10.1038/sj.icb.7100141. Epub 2007 Nov 20.

Abstract

Tolerance to self-antigens within the adaptive immune system is safeguarded, at least in part, through deletion of autoreactive T and B lymphocytes. This deletion can occur during the development of these cells in primary lymphoid organs, the thymus or bone marrow, respectively, or at the mature stage in peripheral lymphoid tissues. Deletion of autoreactive lymphocytes is achieved to a large extent through apoptotic cell death. This review describes current understanding of the mechanisms that mediate apoptosis of autoreactive lymphocytes during their development in primary lymphoid organs and during their activation in the periphery. In particular, we discuss the roles of the proapoptotic Bcl-2 family member Bim and the small family of Nur77-related transcriptional regulators in lymphocyte negative selection. Finally, we speculate on the processes that may lead to the activation of Bim when antigen receptors are activated on autoreactive T or B cells.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Apoptosis / immunology
  • B-Lymphocytes / cytology
  • B-Lymphocytes / immunology*
  • B-Lymphocytes / metabolism*
  • Caspases / immunology
  • Caspases / metabolism
  • Clonal Deletion / immunology
  • Death Domain Receptor Signaling Adaptor Proteins / genetics
  • Death Domain Receptor Signaling Adaptor Proteins / immunology
  • Humans
  • Lymphocyte Activation / genetics
  • Lymphocyte Activation / immunology
  • Mice
  • Proto-Oncogene Proteins c-bcl-2 / genetics
  • Proto-Oncogene Proteins c-bcl-2 / immunology*
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Rats
  • Self Tolerance / genetics
  • Self Tolerance / immunology
  • Signal Transduction / genetics
  • Signal Transduction / immunology*
  • T-Lymphocytes / cytology
  • T-Lymphocytes / immunology*
  • T-Lymphocytes / metabolism*

Substances

  • Death Domain Receptor Signaling Adaptor Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Caspases