Neurosci Lett 2002 Sep 27;330(3):293
Haase C, Schmidt S, Faustmann P.
Department of Neurology, University Hospital Essen, Essen, Germany
In the pathogenesis of multiple sclerosis (MS) genetic factors are known to influence autoreactive T-cell-actions like proliferation and chemotaxis across the blood-brain barrier via chemokine receptors (CCR) and G-protein coupled activating mechanisms.
For the first time, we studied the frequencies of a recently described C825T polymorphism in the G-protein encoding gene for the beta3 subunit (GNB3) together with frequencies of a 32-base-pair deletion in the CCR5 gene (delta32 CCR5) in patients with MS (n=253: relapsing-remitting (RR), n=124 and chronic progressive course, n=129).
Apart from a trend to a reduced frequency of delta32 CCR5 and increased GNB3 825T polymorphism in primary chronic progressive patients, numbers did not reach statistical significance in any group of MS.
These results could not support differences in the genetic background of MS based on that CCR5 mutation or the described GNB3 polymorphism.