J Neuroimmunol 2002 Jan;122(1-2):159-166
Semra YK, Seidi OA, Sharief MK.
Department of Neuroimmunology, Guy's, King's and St. Thomas' School of Medicine, Hodgkin Building, Guy's Hospital, SE1 9RT, London, UK
The pathogenesis of multiple sclerosis (MS) is thought to involve failure of programmed cell death (apoptosis) to eliminate potentially pathogenic, autoreactive T lymphocytes.
This failure may be caused by multiple abnormalities of the cell death machinery.
The inhibitors of apoptosis (IAP) proteins are central regulators of cell death that inhibit apoptosis induced by a variety of stimuli.
In this study, we investigated the dynamics of cellular IAP-1, IAP-2, and X-linked IAP, in resting and mitogen stimulated T lymphocytes from MS patients and relevant controls.
The expression of IAP proteins was significantly higher in mitogen stimulated T lymphocytes from patients with clinically active MS when compared to corresponding expressions from patients with stable MS or from other controls.
Heightened expression of IAP proteins in patients with active MS correlated with clinical features of disease activity, and with T lymphocyte resistance to apoptosis.
In contrast, cellular expression of the anti-apoptosis protein Bcl-2 did not differ between active and stable MS, and was relatively similar between MS patients and controls.
These findings suggest that overexpression
of IAP proteins in stimulated T lymphocytes is a feature of clinically
active multiple sclerosis.
PMID: 11777555 [PubMed - as supplied
PMID: 11777555 [PubMed - as supplied by publisher]