Programmed cell death in HIV infection: dysregulation of BCL-2 and Fas pathways and contribution to AIDS pathogenesis.
In the peripheral immune system, apoptosis is involved in the down-regulation of immune reactions, acting as a homeostatic mechanism to limit the expansion of activated lymphocytes, for example in viral diseases. We previously reported that uninfected T lymphocytes from HIV-infected persons were highly prone to in vitro spontaneous apoptosis which was increased following TCR-dependent or independent activation. The present report reviews recent data suggesting that the chronic stimulation of the immune system in HIV infection induces a dysregulation in the expression of molecules involved in cell survival (Bcl-2) or cell death (Fas), promoting an exacerbated peripheral cell death in blood and lymph nodes, possibly contributing to the loss of both functional cytotoxic and helper T lymphocytes in AIDS.
Gougeon
M L
ML
Départment SIDA et Rétrovirus, Institut Pasteur, Paris, France.
D000163:Acquired Immunodeficiency Syndrome / Q000473:pathology* / Q000503:physiopathology; D017209:Apoptosis / Q000502:physiology*; D019254:Genes, bcl-2 / Q000502:physiology*; D015658:HIV Infections / Q000235:genetics / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D019014:fas Receptor / Q000502:physiology*
D019014:fas Receptor