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1
Multiple sclerosis: possible immunological mechanisms.多发性硬化症:可能的免疫机制。
Clin Immunol Immunopathol. 1989 Jan;50(1 Pt 2):S96-105. doi: 10.1016/0090-1229(89)90116-5.
2
Indictment of the microglia as the villain in multiple sclerosis.将小胶质细胞指认为多发性硬化症的罪魁祸首。
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Multiple sclerosis: immune mechanism and update on current therapies.多发性硬化症:免疫机制及当前治疗进展
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T lymphocytes in the cerebrospinal fluid of patients with multiple sclerosis.多发性硬化症患者脑脊液中的T淋巴细胞。
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7
Studies of autoimmunity in multiple sclerosis.多发性硬化症中的自身免疫研究。
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8
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9
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本文引用的文献

1
Measles virus nucleotide sequences: detection by hybridization in situ.麻疹病毒核苷酸序列:原位杂交检测
Science. 1981 May 8;212(4495):672-5. doi: 10.1126/science.7221554.
2
Intra-blood-brain barrier measles virus antibody synthesis in multiple sclerosis patients.多发性硬化症患者血脑屏障内麻疹病毒抗体的合成
Neurology. 1983 Jan;33(1):45-50. doi: 10.1212/wnl.33.1.45.
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Oligoclonal banding in MS.多发性硬化症中的寡克隆带。
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4
Continual breakdown and regeneration of myelin in progressive multiple sclerosis plaques.进行性多发性硬化斑块中髓鞘的持续分解和再生。
Ann N Y Acad Sci. 1984;436:11-32. doi: 10.1111/j.1749-6632.1984.tb14773.x.
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Ann N Y Acad Sci. 1984;436:52-67. doi: 10.1111/j.1749-6632.1984.tb14775.x.
6
Adoptive transfer of EAE-like lesions from rats with coronavirus-induced demyelinating encephalomyelitis.从患有冠状病毒诱导的脱髓鞘性脑脊髓炎的大鼠身上进行实验性自身免疫性脑脊髓炎样病变的过继转移。
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Slow virus replication: the role of macrophages in the persistence and expression of visna viruses of sheep and goats.慢病毒复制:巨噬细胞在绵羊和山羊维斯纳病毒持续存在及表达中的作用
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Autologous lymphocyte proliferation in multiple sclerosis and the effect of intravenous ACTH.多发性硬化症中的自体淋巴细胞增殖及静脉注射促肾上腺皮质激素的作用。
Ann Neurol. 1981 May;9(5):439-46. doi: 10.1002/ana.410090505.
9
Adoptively transferred chronic relapsing experimental autoimmune encephalomyelitis in the mouse. Neuropathologic analysis.小鼠中过继转移的慢性复发性实验性自身免疫性脑脊髓炎。神经病理学分析。
Lab Invest. 1984 Nov;51(5):534-46.
10
Astrocytes present myelin basic protein to encephalitogenic T-cell lines.星形胶质细胞将髓鞘碱性蛋白呈递给致脑炎T细胞系。
Nature. 1984;307(5948):273-6. doi: 10.1038/307273a0.

多发性硬化症:可能的免疫机制。

Multiple sclerosis: possible immunological mechanisms.

作者信息

McFarland H F, Dhib-Jalbut S

机构信息

Neuroimmunology Branch, NINCDS, Bethesda, Maryland 20892.

出版信息

Clin Immunol Immunopathol. 1989 Jan;50(1 Pt 2):S96-105. doi: 10.1016/0090-1229(89)90116-5.

DOI:10.1016/0090-1229(89)90116-5
PMID:2521315
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7133204/
Abstract

Multiple sclerosis is the principal demyelinating disease of the central nervous system. Although the prevalence of the disease is moderately low, averaging about 40 cases per 100,000 people in high risk areas, it is a particularly devastating disease. It primarily affects young adults, is chronic, and has an unpredictable course. Most discouraging, the cause of the disease is not known and an effective treatment has not been identified. Recently, however, research has yielded some important findings concerning the etiology of MS. Much evidence now points to an immunological process as one of the major elements in the disease. It is also likely that an environmental influence, possibly an infectious process, may contribute to the disease. Finally, it is now certain that genetic makeup influences susceptibility to the disease. At present, the strongest evidence is for a polygenic effect, not the effect of a single gene or gene locus. This review will examine some of the possible immunologically mediated disease processes that could be involved in MS, especially those that could account for a role for infectious and genetic factors in the disease.

摘要

多发性硬化症是中枢神经系统主要的脱髓鞘疾病。尽管该病的患病率适中偏低,在高危地区平均每10万人中约有40例,但它是一种特别具有破坏性的疾病。它主要影响年轻人,病程慢性且不可预测。最令人沮丧的是,该病的病因不明,也尚未确定有效的治疗方法。然而,最近的研究在多发性硬化症的病因方面取得了一些重要发现。现在有很多证据表明免疫过程是该疾病的主要因素之一。环境影响,可能是感染过程,也可能导致该病。最后,现在可以确定的是,基因构成会影响对该病的易感性。目前,最有力的证据支持多基因效应,而非单一基因或基因位点的效应。本综述将探讨一些可能参与多发性硬化症的免疫介导疾病过程,尤其是那些可以解释感染和遗传因素在该疾病中作用的过程。