Association of Macrophage Migration Inhibitory Factor Gene Promoter Polymorphisms with Multiple Sclerosis in Turkish Patients

被引:26
作者
Akcali, A. [1 ]
Pehlivan, S. [2 ]
Pehlivan, M. [3 ]
Sever, T. [2 ]
Neyal, M. [1 ]
机构
[1] Gaziantep Univ, Fac Med, Dept Neurol, Gaziantep, Turkey
[2] Gaziantep Univ, Fac Med, Dept Med Biol & Genet, Gaziantep, Turkey
[3] Gaziantep Univ, Fac Med, Dept Haematol, Gaziantep, Turkey
关键词
MULTIPLE SCLEROSIS; MIGRATION INHIBITORY FACTOR (MIF); PROMOTER POLYMORPHISMS; ONSET AGE; POLYMERASE CHAIN REACTION RESTRICTION FRAGMENT LENGTH POLYMORPHISM (PCR-RFLP); EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; FACTOR MIF; THERAPEUTIC TARGET; RAT-BRAIN; EXPRESSION; CELLS; ARTHRITIS; CYTOKINE; IDENTIFICATION; RECEPTOR;
D O I
10.1177/147323001003800108
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Elevated levels of macrophage migration inhibitory factor (MIF) have been observed in the cerebrospinal fluid of patients with multiple sclerosis. This study was designed to determine if MIF gene polymorphisms are associated with multiple sclerosis and disease severity. In total, 120 relapsing-remitting patients with multiple sclerosis and 120 control subjects were enrolled in the study. There was a statistically significant increase in the MIF -173 CC genotype in patients with multiple sclerosis compared with the control subjects. The MIF -794 6/7 genotype had a significantly lower progression index compared with MIF -794 6/6. Patients with the MIF -173 CC genotype had a significantly lower age of disease onset compared with those with the MIF -173 CG and MIF -173 GG genotypes. Additionally, patients with the MIF -794 5/6 genotype had a significantly later age of disease onset. This study indicates that the MIF -173 CC genotype may cause susceptibility to multiple sclerosis in the white Turkish population and a younger age of disease onset is associated with this polymorphism.
引用
收藏
页码:69 / 77
页数:9
相关论文
共 37 条
[1]  
Amoli MM, 2002, J RHEUMATOL, V29, P1671
[2]   An essential regulatory role for macrophage migration inhibitory factor in T-cell activation [J].
Bacher, M ;
Metz, CN ;
Calandra, T ;
Mayer, K ;
Chesney, J ;
Lohoff, M ;
Gemsa, D ;
Donnelly, T ;
Bucala, R .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (15) :7849-7854
[3]   MIF IS A PITUITARY-DERIVED CYTOKINE THAT POTENTIATES LETHAL ENDOTOXEMIA [J].
BERNHAGEN, J ;
CALANDRA, T ;
MITCHELL, RA ;
MARTIN, SB ;
TRACEY, KJ ;
VOELTER, W ;
MANOGUE, KR ;
CERAMI, A ;
BUCALA, R .
NATURE, 1993, 365 (6448) :756-759
[4]   MACROPHAGE IS AN IMPORTANT AND PREVIOUSLY UNRECOGNIZED SOURCE OF MACROPHAGE-MIGRATION INHIBITORY FACTOR [J].
CALANDRA, T ;
BERNHAGEN, J ;
MITCHELL, RA ;
BUCALA, R .
JOURNAL OF EXPERIMENTAL MEDICINE, 1994, 179 (06) :1895-1902
[5]   Macrophage migration inhibitory factor: A regulator of innate immunity [J].
Calandra, T ;
Roger, T .
NATURE REVIEWS IMMUNOLOGY, 2003, 3 (10) :791-800
[6]   MIF AS A GLUCOCORTICOID-INDUCED MODULATOR OF CYTOKINE PRODUCTION [J].
CALANDRA, T ;
BERNHAGEN, J ;
METZ, CN ;
SPIEGEL, LA ;
BACHER, M ;
DONNELLY, T ;
CERAMI, A ;
BUCALA, R .
NATURE, 1995, 377 (6544) :68-71
[7]   Functional and prognostic relevance of the-173 polymorphism of the macrophage migration inhibitory factor gene in systemic-onset juvenile idiopathic arthritis [J].
De Benedetti, F ;
Meazza, C ;
Vivarelli, M ;
Rossi, F ;
Pistorio, A ;
Lamb, R ;
Lunt, M ;
Thomson, W ;
Ravelli, A ;
Donn, R ;
Martini, A .
ARTHRITIS AND RHEUMATISM, 2003, 48 (05) :1398-1407
[8]   Development of chronic colitis is dependent on the cytokine MIF [J].
de Jong, YP ;
Abadia-Molina, AC ;
Satoskar, AR ;
Clarke, K ;
Rietdijk, ST ;
Faubion, WA ;
Mizoguchi, E ;
Metz, CN ;
Al Sahli, M ;
ten Hove, T ;
Keates, AC ;
Lubetsky, JB ;
Farrell, RJ ;
Michetti, P ;
van Deventer, SJ ;
Lolis, E ;
David, JR ;
Bhan, AK ;
Terhorst, C .
NATURE IMMUNOLOGY, 2001, 2 (11) :1061-1066
[9]   In vivo blockade of macrophage migration inhibitory factor ameliorates acute experimental autoimmune encephalomyelitis by impairing the homing of encephalitogenic T cells to the central nervous system [J].
Denkinger, CM ;
Denkinger, M ;
Kort, JJ ;
Metz, C ;
Forsthuber, TG .
JOURNAL OF IMMUNOLOGY, 2003, 170 (03) :1274-1282
[10]   Genetics of multiple sclerosis [J].
Dyment, DA ;
Ebers, GC ;
Sadovnick, AD .
LANCET NEUROLOGY, 2004, 3 (02) :104-110