Proinflammatory and antiinflammatory cytokines in multiple sclerosis and central nervous system acquired immunodeficiency syndrome.

J E Merrill
{"title":"Proinflammatory and antiinflammatory cytokines in multiple sclerosis and central nervous system acquired immunodeficiency syndrome.","authors":"J E Merrill","doi":"10.1097/00002371-199210000-00004","DOIUrl":null,"url":null,"abstract":"<p><p>While certain cytokines such as interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-alpha), IL-6, and transforming growth factor-beta (TGF-beta) may be involved in pro- and anti-inflammatory events in the central nervous system (CNS) of patients with multiple sclerosis (MS) and CNS acquired immunodeficiency syndrome (AIDS), there is not uniform consensus as to whether they are elevated or even detectable in all compartments of the body such as serum, cerebrospinal fluid (CSF), and tissue. Furthermore, if they are elevated in these diseases, there are no data as to whether they regulate the disease process itself. Myelin damage in MS is a punctate demyelination; in AIDS, it is a diffuse myelin pallor or dysmyelination. Oligodendrocytes are destroyed in MS but not CNS AIDS, suggesting a different mechanism for myelin loss in the two diseases. These different pathologies may provide clues about the role of macrophages, microglia, and/or the toxic products they produce in putatively giving rise to myelin damage. The stimuli that trigger such a destructive response by macrophages or glial cells and/or the regulation of the toxic events in the two diseases we would predict to be different. In MS, an effector cell-mediated lesion production and oligodendrocyte cell destruction seem to occur. We hypothesize that the effector is the inflammatory blood macrophage and/or microglial cell induced and promoted to its cytotoxic activity by a collaboration of neurotransmitters and cytokines. In CNS AIDS, virus-induced toxic products of glia and their diffusion through white and gray matter areas of the brain have been suggested. Such soluble mediators would then compromise metabolic processes of neurons and glia without widespread target cell loss.</p>","PeriodicalId":77209,"journal":{"name":"Journal of immunotherapy : official journal of the Society for Biological Therapy","volume":"12 3","pages":"167-70"},"PeriodicalIF":0.0000,"publicationDate":"1992-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/00002371-199210000-00004","citationCount":"116","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of immunotherapy : official journal of the Society for Biological Therapy","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1097/00002371-199210000-00004","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 116

Abstract

While certain cytokines such as interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-alpha), IL-6, and transforming growth factor-beta (TGF-beta) may be involved in pro- and anti-inflammatory events in the central nervous system (CNS) of patients with multiple sclerosis (MS) and CNS acquired immunodeficiency syndrome (AIDS), there is not uniform consensus as to whether they are elevated or even detectable in all compartments of the body such as serum, cerebrospinal fluid (CSF), and tissue. Furthermore, if they are elevated in these diseases, there are no data as to whether they regulate the disease process itself. Myelin damage in MS is a punctate demyelination; in AIDS, it is a diffuse myelin pallor or dysmyelination. Oligodendrocytes are destroyed in MS but not CNS AIDS, suggesting a different mechanism for myelin loss in the two diseases. These different pathologies may provide clues about the role of macrophages, microglia, and/or the toxic products they produce in putatively giving rise to myelin damage. The stimuli that trigger such a destructive response by macrophages or glial cells and/or the regulation of the toxic events in the two diseases we would predict to be different. In MS, an effector cell-mediated lesion production and oligodendrocyte cell destruction seem to occur. We hypothesize that the effector is the inflammatory blood macrophage and/or microglial cell induced and promoted to its cytotoxic activity by a collaboration of neurotransmitters and cytokines. In CNS AIDS, virus-induced toxic products of glia and their diffusion through white and gray matter areas of the brain have been suggested. Such soluble mediators would then compromise metabolic processes of neurons and glia without widespread target cell loss.

促炎和抗炎细胞因子在多发性硬化和中枢神经系统获得性免疫缺陷综合征中的作用。
虽然某些细胞因子,如白细胞介素-1 (IL-1)、肿瘤坏死因子- α (tnf - α)、IL-6和转化生长因子- β (tgf - β)可能参与多发性硬化症(MS)和中枢神经系统获得性免疫缺陷综合征(AIDS)患者中枢神经系统(CNS)的促炎和抗炎事件,但对于它们是否在血清、脑脊液(CSF)和组织等身体所有部位升高或甚至可检测到,尚无统一的共识。此外,如果它们在这些疾病中升高,则没有数据表明它们是否调节疾病过程本身。多发性硬化症的髓鞘损伤表现为点状脱髓鞘;在艾滋病中,它是弥漫性髓鞘苍白或髓鞘异常。少突胶质细胞在多发性硬化症中被破坏,但在中枢神经系统艾滋病中没有,这表明两种疾病中髓磷脂损失的机制不同。这些不同的病理可能为巨噬细胞、小胶质细胞和/或它们产生的有毒产物在引起髓磷脂损伤中的作用提供线索。巨噬细胞或神经胶质细胞引发这种破坏性反应的刺激和/或我们预测的两种疾病中毒性事件的调节是不同的。在多发性硬化症中,效应细胞介导的病变产生和少突胶质细胞破坏似乎发生。我们假设效应是炎症性血巨噬细胞和/或小胶质细胞在神经递质和细胞因子的协同作用下诱导和促进其细胞毒性活性。在中枢神经系统艾滋病中,病毒诱导的神经胶质毒性产物及其在大脑白质和灰质区域的扩散已被提出。这样的可溶性介质会损害神经元和胶质细胞的代谢过程,而不会造成广泛的靶细胞损失。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信