PROGRAMMED CELL-DEATH IN HIV-INFECTION - DYSREGULATION OF BCL-2 AND FAS PATHWAYS AND CONTRIBUTION TO AIDS PATHOGENESIS

Authors
Citation
Ml. Gougeon, PROGRAMMED CELL-DEATH IN HIV-INFECTION - DYSREGULATION OF BCL-2 AND FAS PATHWAYS AND CONTRIBUTION TO AIDS PATHOGENESIS, Psychoneuroendocrinology, 22, 1997, pp. 33-39
Citations number
44
Categorie Soggetti
Neurosciences,"Endocrynology & Metabolism
Journal title
ISSN journal
03064530
Volume
22
Year of publication
1997
Supplement
1
Pages
33 - 39
Database
ISI
SICI code
0306-4530(1997)22:<33:PCIH-D>2.0.ZU;2-N
Abstract
In the peripheral immune system, apoptosis is involved in the down-reg ulation of immune reactions, acting as a homeostatic mechanism to limi t the expansion of activated lymphocytes, for example in viral disease s. We previously reported that uninfected T lymphocytes from HIV-infec ted persons were highly prone to in vitro spontaneous apoptosis which was increased following TCR-dependent or independent activation. The p resent report reviews recent data suggesting that the chronic stimulat ion of the immune system in HIV infection induces a dysregulation in t he expression of molecules involved in cell survival (Bcl-2) or cell d eath (Fas), promoting an exacerbated peripheral cell death in blood an d lymph nodes, possibly contributing to the loss of both functional cy totoxic and helper T Iymphocytes in AIDS. (C) 1997 Elsevier Science Lt d.