Cytokine producing CD8+ T cells are correlated to MRI features of tissue destruction in MS

被引:27
作者
Killestein, J
Eikelenboom, MJ
Izeboud, T
Kalkers, NF
Adèr, HJ
Barkhof, F
Van Lier, RAW
Uitdehaag, BMJ
Polman, CH
机构
[1] VU Med Ctr, Dept Neurol, Amsterdam, Netherlands
[2] CLB, Dept Clin Viroimmunol, Amsterdam, Netherlands
[3] VU Med Ctr, MS MRI Ctr, Amsterdam, Netherlands
[4] VU Med Ctr, Dept Clin Epidemiol & Biostat, Amsterdam, Netherlands
[5] AMC, Dept Expt Immunol, Amsterdam, Netherlands
关键词
cytokines; multiple sclerosis; CD8(+) T cells; MRI; EDSS;
D O I
10.1016/S0165-5728(03)00265-0
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Specific T-cell subsets and their ability to produce cytokines have been involved in concepts of multiple sclerosis (MS) pathogenesis. Evidence to link cytokine producing T-cell subsets to magnetic resonance imaging (MRI) features of tissue destruction, however, is limited. Cytokine flow cytometry was performed in 124 patients with different subtypes of MS. In a subgroup of 69 patients, from whom longitudinal MRI was available, the ability of circulating types I and 2 helper T cells to produce cytokines was correlated to changes in T1 hypointense and T2 hyperintense lesion load (LL) on brain MRI during 3 years of follow-up. Significant negative correlations were found between baseline CD8(+) T-cell subsets producing IL-2, IL-4 or IL-13 and the change in T1 LL. Subgroup analyses demonstrated that in RRMS, CD8(+) T cells producing IL-2, IL-4 or IL-13, and in PPMS, CD8(+) IL-10(+) T cells correlated negatively with T1 LL. To our knowledge, this study provides the first direct immumophenotypic evidence of cytokine producing CD8+ T cells being directly related to long-term development of MRI features of demyelination and axonal loss. (C) 2003 Elsevier B.V. All rights reserved.
引用
收藏
页码:141 / 148
页数:8
相关论文
共 39 条
[21]   Cell surface bound and soluble adhesion molecules in CSF and blood in multiple sclerosis: correlation with MRI-measures of subclinical disease severity and activity [J].
Kraus, J ;
Engelhardt, B ;
Chatzimanolis, N ;
Bauer, R ;
Tofighi, J ;
Kuehne, BS ;
Laske, C ;
Stolz, E ;
Frielinghaus, P ;
Schaefer, C ;
Blaes, F ;
Traupe, H ;
Kaps, M ;
Oschmann, P .
JOURNAL OF NEUROIMMUNOLOGY, 2002, 122 (1-2) :175-185
[22]   Myelin basic protein-specific T helper 2 (Th2) cells cause experimental autoimmune encephalomyelitis in immunodeficient hosts rather than protect them from the disease [J].
Lafaille, JJ ;
VandeKeere, F ;
Hsu, AL ;
Baron, JL ;
Haas, W ;
Raine, CS ;
Tonegawa, S .
JOURNAL OF EXPERIMENTAL MEDICINE, 1997, 186 (02) :307-312
[23]   Defining the clinical course of multiple sclerosis: Results of an international survey [J].
Lublin, FD ;
Reingold, SC .
NEUROLOGY, 1996, 46 (04) :907-911
[24]   Regulatory T cells control autoimmunity in vivo by inducing apoptotic depletion of activated pathogenic lymphocytes [J].
Madakamutil, LT ;
Maricic, I ;
Sercarz, E ;
Kumar, V .
JOURNAL OF IMMUNOLOGY, 2003, 170 (06) :2985-2992
[25]   Inflammation in multiple sclerosis: the good, the bad, and the complex [J].
Martino, G ;
Adorini, L ;
Rieckmann, P ;
Hillert, J ;
Kallmann, B ;
Comi, G ;
Filippi, M .
LANCET NEUROLOGY, 2002, 1 (08) :499-509
[26]   Medical progress: Multiple sclerosis. [J].
Noseworthy, JH ;
Lucchinetti, C ;
Rodriguez, M ;
Weinshenker, BG .
NEW ENGLAND JOURNAL OF MEDICINE, 2000, 343 (13) :938-952
[27]   An unexpected version of horror autotoxicus: anaphylactic shock to a self peptide [J].
Pedotti, R ;
Mitchell, D ;
Wedemeyer, J ;
Karpuj, M ;
Chabas, D ;
Hattab, EM ;
Tsai, M ;
Galli, SJ ;
Steinman, L .
NATURE IMMUNOLOGY, 2001, 2 (03) :216-222
[28]  
Prat A, 2000, ANN NEUROL, V47, P234, DOI 10.1002/1531-8249(200002)47:2<234::AID-ANA14>3.3.CO
[29]  
2-J
[30]   A genome screen in multiple sclerosis reveals susceptibility loci on chromosome 6p21 and 17q22 [J].
Sawcer, S ;
Jones, HB ;
Feakes, R ;
Gray, J ;
Smaldon, N ;
Chataway, J ;
Robertson, N ;
Clayton, D ;
Goodfellow, PN ;
Compston, A .
NATURE GENETICS, 1996, 13 (04) :464-468