Abstract
Accumulating evidence implicates a failure of myelin-reactive immune cells to undergo apoptosis in the pathological events contributing to multiple sclerosis (MS). We have recently demonstrated that members of the inhibitor of apoptosis (IAP) family of antiapoptotic genes are elevated in peripheral blood immune cells (monocytes, T cells) of patients with aggressive forms of MS (secondary progressive) or those with relapsing-remitting MS suffering a disease replase. These findings suggest that the IAPs may be novel diagnostic markers for distinguishing subtypes of MS. Moreover, antisense-mediated knockdown of the IAP family member known as Xlinked IAP (XIAP) reverses paralysis in an animal model of MS suggesting that treatments targeting XIAP, and perhaps other IAPs, may have utility in the treatment of MS.
Current Drug Discovery Technologies
Title: Targeting Apoptosis to Treat Multiple Sclerosis
Volume: 5 Issue: 1
Author(s): George S. Robertson, Andrea L.O. Hebb, Craig S. Moore and Virender Bhan
Affiliation:
Abstract: Accumulating evidence implicates a failure of myelin-reactive immune cells to undergo apoptosis in the pathological events contributing to multiple sclerosis (MS). We have recently demonstrated that members of the inhibitor of apoptosis (IAP) family of antiapoptotic genes are elevated in peripheral blood immune cells (monocytes, T cells) of patients with aggressive forms of MS (secondary progressive) or those with relapsing-remitting MS suffering a disease replase. These findings suggest that the IAPs may be novel diagnostic markers for distinguishing subtypes of MS. Moreover, antisense-mediated knockdown of the IAP family member known as Xlinked IAP (XIAP) reverses paralysis in an animal model of MS suggesting that treatments targeting XIAP, and perhaps other IAPs, may have utility in the treatment of MS.
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Cite this article as:
Robertson S. George, Hebb L.O. Andrea, Moore S. Craig and Bhan Virender, Targeting Apoptosis to Treat Multiple Sclerosis, Current Drug Discovery Technologies 2008; 5 (1) . https://dx.doi.org/10.2174/157016308783769432
DOI https://dx.doi.org/10.2174/157016308783769432 |
Print ISSN 1570-1638 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6220 |
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