Chemokine receptor CCR5 in interferon-treated multiple sclerosis

被引:14
作者
Sellebjerg, F.
Kristiansen, T. B.
Wittenhagen, P.
Garred, P.
Eugen-Olsen, J.
Frederiksen, J. L.
Sorensen, T. L.
机构
[1] Univ Copenhagen, MS Clin, Glostrup Hosp, Dept Neurol, DK-2600 Glostrup, Denmark
[2] Univ Copenhagen, Hvidovre Hosp, Dept Infect Dis, DK-2650 Hvidovre, Denmark
[3] Univ Copenhagen, Rigshosp, Dept Clin Immun, Copenhagen, Denmark
[4] Univ Copenhagen, Hvidovre Hosp, Clin Res Unit, Hvidovre, Denmark
来源
ACTA NEUROLOGICA SCANDINAVICA | 2007年 / 115卷 / 06期
关键词
CCR5; chemokines; immunogenetics; beta-interferon; monocytes; multiple sclerosis;
D O I
10.1111/j.1600-0404.2007.00826.x
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Objective - To study the relationship between CC chemokine receptor CCR5 expression and disease activity in multiple sclerosis (MS) patients treated with P-interferon (IFN-beta). Methods - The CCR5 angle 32 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-P 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 angle 32 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-beta, but it is possible that monocyte CCR5 expression may be used as a marker of disease activity.
引用
收藏
页码:413 / 418
页数:6
相关论文
共 32 条
[1]   CCR5+ and CXCR3+ T cells are increased in multiple sclerosis and their ligands MIP-1α and IP-10 are expressed in demyelinating brain lesions [J].
Balashov, KE ;
Rottman, JB ;
Weiner, HL ;
Hancock, WW .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (12) :6873-6878
[2]   CC-chemokine receptor 5 polymorphism and age of onset in familial multiple sclerosis [J].
Barcellos, LF ;
Schito, AM ;
Rimmler, JB ;
Vittinghoff, E ;
Shih, A ;
Lincoln, R ;
Callier, S ;
Elkins, MK ;
Goodkin, DE ;
Haines, JL ;
Pericak-Vance, MA ;
Hauser, SL ;
Oksenberg, JR .
IMMUNOGENETICS, 2000, 51 (4-5) :281-288
[3]   The CCR5 deletion mutation fails to protect against multiple sclerosis [J].
Bennetts, BH ;
Teutsch, SM ;
Buhler, MM ;
Heard, RNS ;
Stewart, GJ .
HUMAN IMMUNOLOGY, 1997, 58 (01) :52-59
[4]   B cells and professional APCs recruit regulatory T cells via CCL4 [J].
Bystry, RS ;
Aluvihare, V ;
Welch, KA ;
Kallikourdis, M ;
Betz, AG .
NATURE IMMUNOLOGY, 2001, 2 (12) :1126-1132
[5]   The chemokine receptor CCR5 deletion mutation is associated with MS in HLA-DR4-positive Russians [J].
Favorova, OO ;
Andreewski, TV ;
Boiko, AN ;
Sudomoina, MA ;
Alekseenkov, AD ;
Kulakova, OG ;
Slanova, AV ;
Gusev, EI .
NEUROLOGY, 2002, 59 (10) :1652-1655
[6]   Association of CCR5 Δ32 deletion with early death in multiple sclerosis [J].
Gade-Andavolu, R ;
Comings, DE ;
MacMurray, J ;
Rostamkhani, M ;
Cheng, LSC ;
Tourtellotte, WW ;
Cone, LA .
GENETICS IN MEDICINE, 2004, 6 (03) :126-131
[7]   Chemokine inhibition - why, when, where, which and how? [J].
Johnson, Z ;
Power, CA ;
Weiss, C ;
Rintelen, F ;
Ji, H ;
Ruckle, T ;
Camps, M ;
Wells, TNC ;
Schwarz, MK ;
Proudfoot, AEI ;
Rommel, C .
BIOCHEMICAL SOCIETY TRANSACTIONS, 2004, 32 :366-377
[8]   A mutated CCR5 gene may have favorable prognostic implications in MS [J].
Kantor, R ;
Bakhanashvili, M ;
Achiron, A .
NEUROLOGY, 2003, 61 (02) :238-240
[9]   Interferon-β1a does not reduce expression of CCR5 and CXCR3 on circulating T cells [J].
Kivisäkk, P ;
Cotleur, AC ;
Lee, JC ;
Rudick, RA ;
Ransohoff, RM .
JOURNAL OF NEUROIMMUNOLOGY, 2003, 141 (1-2) :150-154
[10]   Microarray analysis identifies interferon β-regulated genes in multiple sclerosis [J].
Koike, F ;
Satoh, J ;
Miyake, S ;
Yamamoto, T ;
Kawai, M ;
Kikuchi, S ;
Nomura, K ;
Yokoyama, K ;
Ota, K ;
Kanda, T ;
Fukazawa, T ;
Yamamura, T .
JOURNAL OF NEUROIMMUNOLOGY, 2003, 139 (1-2) :109-118