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.
Centre d'Immunologie et de Biologie Parasitaire, INSERM U 167-CNRS 624, Institut Pasteur, Lille, France.
J C
JC
Ameisen
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A
Capron
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