Another differential for mutism
Another differential for mutism
复制标题
沉默症的另一个区别
作者：
Justin McArthur;Bruce Moffatt
我想支持Dale McFarlin博士在他的社论“干扰素在多发性硬化症中的应用”中提出的关于在多发性硬化症患者的治疗中使用干扰素的注意事项。人们必须关注天然干扰素中的“污染”物质甚至使用重组DNA技术生产的干扰素的免疫学和可能的临床副作用。也许同样重要的是，人们还必须考虑免疫反应的有效调节剂的生物效应本身可能是有害的。已经发现，中枢和外周神经系统中的大多数细胞具有很少或没有I型或I1型主要组织相容性复合物抗原（MHC）[2，4，5，11}。γ干扰素已显示在体外和体内诱导包括少突胶质细胞、星形胶质细胞、巨噬细胞小胶质细胞和神经元在内的几种细胞类型上的I型（人类中的HLA-A和-B，小鼠中的HLA-B）MHC抗原（9，12）。这些抗原的存在将使这些细胞类型对针对携带病毒抗原或自身抗原的细胞毒性T细胞反应更敏感（137.γ-干扰素还可增强细胞毒性T细胞克隆的产生[3}。一些研究小组还报道，γ-干扰素增强星形胶质细胞和巨噬细胞小胶质细胞上的I1型MHC抗原（Ia或DR）（1，91）以及许多非神经元细胞类型，包括内皮细胞、T淋巴细胞和单核细胞巨噬细胞的其他亚群[ 1，31]。据报道，在患有多发性硬化症的患者的中枢神经系统中的一些星形胶质细胞和内皮细胞以及血管周围巨噬细胞和巨噬细胞-小胶质细胞中以及在患有实验性过敏性脑脊髓炎的动物中，DR阳性增加。事实上，管理的抗体Ia抑制实验性过敏性脑脊髓炎I8 - 7的发展。DR的存在理论上允许这些细胞呈递抗原并在神经系统中自我维持免疫病理反应。已经证明了通过星形胶质细胞富集培养物将这种抗原呈递给致敏淋巴细胞[ 11]。此外，γ-干扰素还可能激活其他单核巨噬细胞依赖性功能，包括免疫吞噬作用，并增加自然杀伤细胞活性（131，这两种作用均可能导致组织损伤增强。基于上述考虑，我们可以提出这样的假设，即γ-干扰素实际上可能是多发性硬化症患者的禁忌症。
I would like to support the note of caution on the use of interferons in the treatment of patients with multiple sclerosis raised by Dr Dale McFarlin in his editorial, “Use of Interferon in Multiple Sclerosis” {GI. One must be concerned about immunological and possible clinical side effects of “contaminating” materials in natural interferons and even interferon produced using recombinant DNA technology. Perhaps as important, one must also consider the possibility that the biological effect of a potent modifier of the immune response could itself be harmful. It has been found that most cells in the central and peripheral nervous system have little or no type I or I1 major histocompatibility complex antigens (MHC) [2,4, 5, ll}. yInterferon has been shown to induce type I (HLA-A and -B in humans, Hz in mice) MHC antigens on several cell types including oligodendrocytes, astrocytes, macrophage microglia, and neurons in vitro and in vivo {9, 12). The presence of such antigens would render these cell types more susceptible to cytotoxic T-cell reactions directed at harbored viral antigens or autoantigens (1 37. y-Interferon may also enhance the generation of cytotoxic T-cell clones [3}. It has also been reported by some groups that y-interferon enhances type I1 MHC antigens (Ia or DR) on astrocytes and macrophage microglia (1, 91 as well as many nonneuronal cell types including endothelium, T lymphocytes, and other subpopulations of monocyte macrophags [ 1, 31. It has been reported that there is an increase in DR positivity among some astrocytes and endothelial cells as well as perivascular macrophages and macrophage-microglia in the central nervous system of patients with multiple sclerosis {lo] and in animals with experimental allergic encephalomyelitis f71. Indeed, administration of antibodies to Ia inhibits the development of experimental allergic encephalomyelitis I8 7. The presence of DR would allow these cells theoretically to present antigen and to self-perpetuate an immunopathological reaction in the nervous system. Such antigen presentation to sensitized lymphocytes by astrocyte-enriched cultures has been demonstrated [ 11. In addition, y-interferon may activate other monocyte macrophage-dependent functions, including immune phagocytosis, and increase natural killer cell activity (131, both of which could lead to enhanced tissue damage. Based on the above considerations, one could offer the hypothesis that y-interferon might actually be contraindicated in patients with multiple sclerosis.
实验性过敏性脑脊髓炎的免疫病理学。
DOI：
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发表时间：
1984
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
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作者：
Sobel,RA;Blanchette,BW;Bhan,AK;Colvin,RB
通讯作者：
Colvin,RB