Premium
Chemokine receptor CCR5 in interferon‐treated multiple sclerosis
Author(s) -
Sellebjerg F.,
Kristiansen T. B.,
Wittenhagen P.,
Garred P.,
EugenOlsen J.,
Frederiksen J. L.,
Sørensen T. L.
Publication year - 2007
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.2007.00826.x
Subject(s) - multiple sclerosis , chemokine receptor ccr5 , pathogenesis , chemokine receptor , immunology , monocyte , receptor , chemokine , genotype , allele , flow cytometry , medicine , interferon , interferon gamma , biology , cytokine , gene , genetics
Objective – To study the relationship between CC chemokine receptor CCR5 expression and disease activity in multiple sclerosis (MS) patients treated with β ‐interferon (IFN‐ β ). Methods – The CCR5 Δ32 allele and a CCR5 promoter polymorphism associated with cell surface expression of CCR5 were analyzed in 109 patients with relapsing–remitting MS treated with IFN‐ β who were followed clinically for 1 year. Cellular CCR5 expression was measured by flow cytometry. Results – Patients with MS had a higher percentage of CCR5‐positive monocytes than healthy controls. Increased monocyte expression of CCR5 correlated weakly with an increased short‐term relapse risk but there was no relationship between CCR5 Δ32 allele and CCR5 promoter polymorphism genotypes and relapse risk. Conclusions – The results do not support a major role of CCR5 in the pathogenesis of relapses in MS patients treated with IFN‐ β , but it is possible that monocyte CCR5 expression may be used as a marker of disease activity.