Macrophage migration inhibitory factor in the cerebrospinal fluid of patients with conventional and optic-spinal forms of multiple sclerosis and neuro-Behcet's disease

Macrophage migration inhibitory factor in the cerebrospinal fluid of patients with conventional and optic-spinal forms of multiple sclerosis and neuro-Behcet's disease
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DOI:
10.1016/s0022-510x(00)00397-x
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发表时间:
2000-10-01
影响因子:
4.4
通讯作者:
Nishihira, J
Nishihira, J
中科院分区:
医学3区
文献类型:
--
作者:
Niino, M;Ogata, A;Nishihira, J

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巨噬细胞移动抑制因子(MIF)越来越被认为是免疫和炎症反应的重要调节因子。它由活化的T淋巴细胞和巨噬细胞释放,并上调这些细胞的促炎活性。MIF是抗原和丝裂原驱动的T细胞活化所必需的,并刺激巨噬细胞释放细胞因子和一氧化氮。基于最近的建议,即药物调制的MIF生产和中和其活性可能有重要的意义,治疗各种自身免疫性或炎症性疾病,我们确定了患者的脑脊液(CSF)中的MIF水平与常规形式的多发性硬化症(C-MS)和视神经脊髓型多发性硬化症(OpS-MS),神经白塞氏病(NBD)。作为对照,使用患有非炎性神经系统疾病(NIND)的患者的CSF。CSF样品中的MIF浓度在复发的C-MS病例中显著升高(4.13+/-1.07 ng/ml)(平均值+/-S.D.)。与对照组相比(2.38 ± 0.60 ng/ml)(P < 0.0001),而缓解期C-MS患者CSF中的MIF没有升高(2.65 ± 0.67 ng/ml)。复发期OpS-MS患者CSF中MIF浓度(5.53 ± 1.74ng/ml)高于复发期C-MS患者(P < 0.05)。NBD患者脑脊液中MIF浓度为7.47 ± 5.61ng/ml,与对照组比较差异有显著性(P < 0.01),且与脑脊液细胞计数呈良好的相关性(r = 0.910,P < 0.005)。这些结果表明,MIF可能在中枢神经系统的免疫介导的疾病中起关键作用,并且MIF可能用于研究C-MS和OpS-MS之间的差异。
Macrophage migration inhibitory factor (MIF) is becoming increasingly recognized as an important regulator of immune and inflammatory responses. It is released by activated T lymphocytes and macrophages and up-regulates the proinflammatory activity of these cells. MIF is required for antigen- and mitogen-driven T cell activation, and stimulates macrophages to release cytokines and nitric oxide. On the basis of the recent suggestion that pharmacological modulation of MIF production and neutralization of its activity may have important implications for treatment of a variety of autoimmune or inflammatory conditions, we determined the level of MIF in the cerebrospinal fluid (CSF) of patients with conventional-form multiple sclerosis (C-MS) and optic-spinal form multiple sclerosis (OpS-MS), and neuro-Behcet's disease (NBD). As control, the CSF of patients with non-inflammatory neurological diseases (NIND) was used. The concentration of MIF in CSF samples was significantly elevated in relapsed cases of C-MS (4.13+/-1.07 ng/ml) (mean+/-S.D.) compared with control samples (2.38+/-0.60 ng/ml) (P < 0.0001), whereas MIF in the CSF of C-MS patients in remission was not elevated (2.65+/-0.67 ng/ml). The concentration of MIF in the CSF of OpS-MS patients in relapse (5.53+/-1.74 ng/ml) was higher than that of patients with C-MS in relapse (P < 0.05). In NBD patients, the concentration of MIF in CSF was significantly elevated (7.47+/-5.61 ng/ml) compared with control samples (P < 0.01) and correlated well with cell count in these samples (r = 0.910, P < 0.005). These results suggest that MIF may play a pivotal role in immune-mediated diseases of the central nervous system, and that MIF may be useful in the study of differences between C-MS and OpS-MS. (C) 2000 Published by Elsevier Science B.V.