Cell dysfunction and depletion in AIDS: the programmed cell death hypothesis

Immunol Today. 1991 Apr;12(4):102-5. doi: 10.1016/0167-5699(91)90092-8.

Abstract

Normal immature thymocytes respond to activation by undergoing programmed cell death (apoptosis), a physiological deletion mechanism involved in the selection of the T-cell repertoire. In this article, Jean Claude Ameisen and André Capron suggest that inappropriate induction of a form of programmed T-cell death could account for both qualitative and quantitative helper T-cell defects of HIV-infected patients. A model of AIDS pathogenesis is presented that may explain several features of HIV infection, including evolution of the disease and the development of defects in nonimmunological organs.

Publication types

  • Review

MeSH terms

  • AIDS Dementia Complex / pathology
  • Acquired Immunodeficiency Syndrome / pathology*
  • CD4-Positive T-Lymphocytes / drug effects
  • CD4-Positive T-Lymphocytes / immunology
  • CD4-Positive T-Lymphocytes / pathology*
  • Cell Survival* / drug effects
  • Endodeoxyribonucleases / biosynthesis
  • Endodeoxyribonucleases / physiology
  • Gene Expression Regulation
  • HIV / physiology
  • HIV Envelope Protein gp120 / physiology
  • Hematopoietic Stem Cells / pathology
  • Lymphocyte Activation / drug effects
  • Mitogens / pharmacology
  • Models, Biological
  • Signal Transduction

Substances

  • HIV Envelope Protein gp120
  • Mitogens
  • Endodeoxyribonucleases