Ontwikkelingen Alfa b Crystalline
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Giechel
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Robbie
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Robbie
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Cæsar
[URL="http://www.iocob.nl/multiple-sclerose/m ... lline.html"]MS patienten te snel blij gemaakt[/URL] artikel september 2007
[QUOTE][B]Commentaar IOCOB[/B]
Zelfs mocht de stof uiteindelijk toch werken, dan duurt het minstens 6-8 jaar voordat de stof op de markt zal verschijnen![/QUOTE]
Zitten nu op 9 jaar ?
[QUOTE][B]Commentaar IOCOB[/B]
Zelfs mocht de stof uiteindelijk toch werken, dan duurt het minstens 6-8 jaar voordat de stof op de markt zal verschijnen![/QUOTE]
Zitten nu op 9 jaar ?
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Robbie
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Leonard
ik ben bang dat dit pad niet gaat werken, zie wat Michael Pender hier over schrijft (uit: [url]http://www.nature.com/cti/journal/v3/n1 ... 1425a.html[/url] ):
αB-crystallin or ‘mistaken self’ hypothesis
The αB-crystallin or ‘mistaken self’ hypothesis proposes that exposure to infectious agents induces the expression of αB-crystallin, a small heat-shock protein, in lymphoid cells and that the immune system mistakes self αB-crystallin for a microbial antigen and generates a CD4+ T-cell response, which then attacks αB-crystallin derived from oligodendrocytes, with resultant demyelination.137 αB-crystallin is reportedly an immunodominant antigen of CNS myelin from MS patients, which is expressed in oligodendrocytes and myelin in early MS lesions, but not in normal white matter.137 An essential aspect of this hypothesis is that infection of the CNS by a microbial agent, which may not be the same as the one inducing αB-crystallin in lymphoid cells, upregulates the expression of αB-crystallin in oligodendrocytes and provides other ‘danger’ signals in the CNS, thereby allowing inflammation to develop. Although the hypothesis is not specific for EBV, EBV is a potential candidate because it induces the expression of αB-crystallin in B cells, which present the protein to CD4+ T cells in a human leukocyte antigen-DR-restricted manner.138 By itself, this hypothesis cannot explain the initial development and subsequent persistence of inflammation in the CNS but it might account for how CD4+ T cells target oligodendrocytes and myelin after initiation of CNS inflammation.
het is jammer voor de onderzoekers die jaren hier aan hebben gewerkt.
αB-crystallin or ‘mistaken self’ hypothesis
The αB-crystallin or ‘mistaken self’ hypothesis proposes that exposure to infectious agents induces the expression of αB-crystallin, a small heat-shock protein, in lymphoid cells and that the immune system mistakes self αB-crystallin for a microbial antigen and generates a CD4+ T-cell response, which then attacks αB-crystallin derived from oligodendrocytes, with resultant demyelination.137 αB-crystallin is reportedly an immunodominant antigen of CNS myelin from MS patients, which is expressed in oligodendrocytes and myelin in early MS lesions, but not in normal white matter.137 An essential aspect of this hypothesis is that infection of the CNS by a microbial agent, which may not be the same as the one inducing αB-crystallin in lymphoid cells, upregulates the expression of αB-crystallin in oligodendrocytes and provides other ‘danger’ signals in the CNS, thereby allowing inflammation to develop. Although the hypothesis is not specific for EBV, EBV is a potential candidate because it induces the expression of αB-crystallin in B cells, which present the protein to CD4+ T cells in a human leukocyte antigen-DR-restricted manner.138 By itself, this hypothesis cannot explain the initial development and subsequent persistence of inflammation in the CNS but it might account for how CD4+ T cells target oligodendrocytes and myelin after initiation of CNS inflammation.
het is jammer voor de onderzoekers die jaren hier aan hebben gewerkt.