CONTRASTING EFFECTS OF ALPHA, BETA, AND GAMMA INTERFERONS ON NONSPECIFIC SUPPRESSOR FUNCTION IN MULTIPLE-SCLEROSIS

被引:55
作者
NORONHA, A [1 ]
TOSCAS, A [1 ]
JENSEN, MA [1 ]
机构
[1] UNIV CHICAGO,INST BRAIN RES,CHICAGO,IL 60637
关键词
D O I
10.1002/ana.410310119
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Interferons are biological molecules with antiviral, antiproliferative, and immunomodulatory actions. Interferon alpha (IFN-alpha) and -beta are potentially useful in the treatment of multiple sclerosis (MS). IFN-gamma, in contrast, increases the frequency of exacerbations of MS. In this study, we compared the effect of recombinant human IFN-alpha, -beta, and -gamma on suppressor function in patients with MS. Nonspecific suppressor cell function, measured in a concanavalin A suppressor assay, was significantly decreased in 16 patients with progressive MS (mean percent suppression +/- SEM, 14.4 +/- 5.5 in patients with MS, 33.5 +/- 4.8 in 16 normal subjects; p < 0.001). Recombinant human IFN-beta augmented suppressor function in MS to 45.4 +/- 5.1% (p < 0.001) and in control subjects to 56.8 +/- 3.8% (p < 0.001). Similarly, recombinant human IFN-alpha improved suppression in MS to 43.0 +/- 5.6% (p < 0.001) and in control subjects to 51.1 +/- 5.9% (p < 0.001). In contrast, recombinant human IFN-gamma had no effect on suppressor function in patients with MS and in control subjects. This study shows that IFN-alpha and -beta augment deficient suppressor function in MS, whereas IFN-gamma has no effect on suppressor function in the progressive phase of the disease.
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页码:103 / 106
页数:4
相关论文
共 34 条
[1]   ACTIVATED SUPPRESSOR-CELL FUNCTION IN MULTIPLE-SCLEROSIS - CLINICAL CORRELATIONS [J].
ANTEL, J ;
BROWN, M ;
NICHOLAS, MK ;
BLAIN, M ;
NORONHA, A ;
REDER, A .
JOURNAL OF NEUROIMMUNOLOGY, 1988, 17 (04) :323-330
[2]  
ARNASON BGW, 1978, ANN INST PASTEUR IMM, VC129, P159
[3]   ACTIVATION OF A SUPPRESSOR T-CELL PATHWAY BY INTERFERON [J].
AUNE, TM ;
PIERCE, CW .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES, 1982, 79 (12) :3808-3812
[4]   INTERFERON-BETA IMPAIRS INDUCTION OF HLA-DR ANTIGEN EXPRESSION IN CULTURED ADULT HUMAN ASTROCYTES [J].
BARNA, BP ;
CHOU, SM ;
JACOBS, B ;
YENLIEBERMAN, B ;
RANSOHOFF, RM .
JOURNAL OF NEUROIMMUNOLOGY, 1989, 23 (01) :45-53
[5]   INCREASED PRODUCTION OF INTERFERON GAMMA AND TUMOR NECROSIS FACTOR PRECEDES CLINICAL MANIFESTATION IN MULTIPLE-SCLEROSIS - DO CYTOKINES TRIGGER OFF EXACERBATIONS [J].
BECK, J ;
RONDOT, P ;
CATINOT, L ;
FALCOFF, E ;
KIRCHNER, H ;
WIETZERBIN, J .
ACTA NEUROLOGICA SCANDINAVICA, 1988, 78 (04) :318-323
[6]  
BELLAMY AS, 1985, CLIN EXP IMMUNOL, V61, P248
[7]  
CAMENGA DL, 1986, ARCH NEUROL-CHICAGO, V43, P1239
[8]   CHARACTERIZATION OF 3 MONOCLONAL-ANTIBODIES THAT RECOGNIZE THE INTERFERON-ALPHA-2 RECEPTOR [J].
COLAMONICI, OR ;
DALESSANDRO, F ;
DIAZ, MO ;
GREGORY, SA ;
NECKERS, LM ;
NORDAN, R .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (18) :7230-7234
[9]   ADHESION OF T-LYMPHOBLASTS TO EPIDERMAL-KERATINOCYTES IS REGULATED BY INTERFERON-GAMMA AND IS MEDIATED BY INTERCELLULAR-ADHESION MOLECULE-1 (ICAM-1) [J].
DUSTIN, ML ;
SINGER, KH ;
TUCK, DT ;
SPRINGER, TA .
JOURNAL OF EXPERIMENTAL MEDICINE, 1988, 167 (04) :1323-1340
[10]  
FIERZ W, 1985, J IMMUNOL, V134, P3785