Cell dysfunction and depletion in AIDS: the programmed cell death hypothesis.
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.
Ameisen
J C
JC
Centre d'Immunologie et de Biologie Parasitaire, INSERM U 167-CNRS 624, Institut Pasteur, Lille, France.
Capron
A
A
D015526:AIDS Dementia Complex / Q000473:pathology; D000163:Acquired Immunodeficiency Syndrome / Q000473:pathology*; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects / Q000276:immunology / Q000473:pathology*; D002470:Cell Survival / Q000187:drug effects; D004706:Endodeoxyribonucleases / Q000096:biosynthesis / Q000502:physiology; D005786:Gene Expression Regulation; D006678:HIV / Q000502:physiology; D015699:HIV Envelope Protein gp120 / Q000502:physiology; D006412:Hematopoietic Stem Cells / Q000473:pathology; D008213:Lymphocyte Activation / Q000187:drug effects; D008934:Mitogens / Q000494:pharmacology; D008954:Models, Biological; D015398:Signal Transduction
D015699:HIV Envelope Protein gp120; D008934:Mitogens; D004706:Endodeoxyribonucleases