Decreases in T-cell tumor necrosis factor α binding with interferon beta treatment in patients with multiple sclerosis

被引:9
作者
Bongioanni, P
Mosti, S
Moscato, G
Lombardo, F
Manildo, C
Meucci, G
机构
[1] Univ Pisa, Dept Neurosci, Neurol Sect, I-56100 Pisa, Italy
[2] Univ Turin, Inst Clin Med, Turin, Italy
关键词
D O I
10.1001/archneur.56.1.71
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Objective: To investigate the effects of interferon beta treatment on T-cell tumor necrosis factor alpha (TNF-alpha) binding (which is a possible marker for T-cell-dependent immune function) in patients with multiple sclerosis. Design: The TNF-alpha binding on T lymphocytes from patients with stable relapsing-remitting multiple sclerosis was assayed before and 3 and 6 months after the start of treatment with interferon beta. Setting: The study was performed on ambulatory patients in a tertiary care center. Patients: Eighteen patients with clinically definite stable relapsing-remitting multiple sclerosis (13 women and 5 men; mean [+/- SD] age, 32.6 +/- 7.1 years) were selected consecutively. Clinical status was defined according to the Expanded Disability Status Scale. All patients were treated with 8 X 10(6) U of interferon beta-1b subcutaneously every other day. Eighteen age- and sex-matched healthy subjects, with no family history of neuropsychiatric disorders, served as controls. Results: T lymphocytes from untreated patients with multiple sclerosis had significantly more TNF-or receptors than those from controls (mean +/- SE, 837 +/- 33 vs 135 +/- 5 receptors per cell). After 3 months of treatment with interferon beta-1b, they showed a significant decrease (P<.001) in TNF-alpha binding (452 +/- 29 receptors per cell). After 6 months, T-cell TNF-alpha maximal receptor numbers were even lower (345 +/- 35 receptors per cell). Conclusion: Given that increased TNF-alpha binding might be linked to lymphocyte activation, our data demonstrate that a major effect of interferon beta-1b treatment is to decrease T-cell activation.
引用
收藏
页码:71 / 78
页数:8
相关论文
共 89 条
[11]  
BONGIOANNI P, 1991, J CHEMOTHER, V3, P32
[12]   T-CELL SUBPOPULATIONS IN BLOOD AND CEREBROSPINAL-FLUID OF MULTIPLE-SCLEROSIS PATIENTS - EFFECT OF CYCLOPHOSPHAMIDE [J].
BRINKMAN, CJJ ;
NILLESEN, WM ;
HOMMES, OR .
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY, 1983, 29 (03) :341-348
[13]   IDENTIFICATION OF 2 TYPES OF TUMOR-NECROSIS-FACTOR RECEPTORS ON HUMAN CELL-LINES BY MONOCLONAL-ANTIBODIES [J].
BROCKHAUS, M ;
SCHOENFELD, HJ ;
SCHLAEGER, EJ ;
HUNZIKER, W ;
LESSLAUER, W ;
LOETSCHER, H .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (08) :3127-3131
[14]   IFN-beta(1b) treatment of relapsing multiple sclerosis has no effect on CD3-induced inflammatory or counterregulatory anti-inflammatory cytokine secretion ex vivo after nine months [J].
Brod, SA ;
Nelson, LD ;
Khan, M ;
Wolinsky, JS .
INTERNATIONAL JOURNAL OF NEUROSCIENCE, 1997, 90 (1-2) :135-144
[15]   Interferon-beta(1b) treatment decreases tumor necrosis factor-alpha and increases interleukin-6 production in multiple sclerosis [J].
Brod, SA ;
Marshall, GD ;
Henninger, EM ;
Sriram, S ;
Khan, M ;
Wolinsky, JS .
NEUROLOGY, 1996, 46 (06) :1633-1638
[16]  
Byskosh P V, 1996, Mult Scler, V1, P262
[17]   VLA-4 expression on peripheral blood lymphocytes is downregulated after treatment of multiple sclerosis with interferon beta [J].
Calabresi, PA ;
Pelfrey, CM ;
Tranquill, LR ;
Maloni, H ;
McFarland, HF .
NEUROLOGY, 1997, 49 (04) :1111-1116
[18]   Increases in soluble VCAM-1 correlate with a decrease in MRI lesions in multiple sclerosis treated with interferon beta-1b [J].
Calabresi, PA ;
Tranquill, LR ;
Dambrosia, JM ;
Stone, LA ;
Maloni, H ;
Bash, CN ;
Frank, JA ;
McFarland, HF .
ANNALS OF NEUROLOGY, 1997, 41 (05) :669-674
[19]  
CALOPA M, 1995, ACTA NEUROL SCAND, V92, P361
[20]  
Chofflon M, 1992, Eur Cytokine Netw, V3, P523