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1
Nitric oxide contributes to resistance of the Brown Norway rat to experimental autoimmune encephalomyelitis.一氧化氮有助于棕色挪威大鼠对实验性自身免疫性脑脊髓炎产生抵抗力。
Am J Pathol. 2005 Jan;166(1):147-57. doi: 10.1016/S0002-9440(10)62240-7.
2
Limiting-dilution analysis of the frequency of myelin basic protein-reactive T cells in Lewis, PVG/c and BN rats. Implication for susceptibility to autoimmune encephalomyelitis.对Lewis、PVG/c和BN大鼠中髓鞘碱性蛋白反应性T细胞频率的有限稀释分析。对自身免疫性脑脊髓炎易感性的影响。
Immunology. 1990 Feb;69(2):215-21.
3
The innate immune response to adjuvants dictates the adaptive immune response to autoantigens.对佐剂的天然免疫反应决定了对自身抗原的适应性免疫反应。
J Neuropathol Exp Neurol. 2008 Jun;67(6):543-54. doi: 10.1097/NEN.0b013e31817713cc.
4
Allergic encephalomyelitis in the reputedly resistant Brown Norway strain of rats.在据称具有抗性的大鼠棕色挪威品系中发生的变应性脑脊髓炎。
J Immunol. 1975 Feb;114(2 Pt 1):597-601.
5
In situ Ia expression on brain cells in the rat: autoimmune encephalomyelitis-resistant strain (BN) and susceptible strain (Lewis) compared.大鼠脑细胞原位Ia表达：自身免疫性脑脊髓炎抗性品系（BN）与易感品系（Lewis）的比较。
Immunology. 1989 Apr;66(4):621-7.
6
Nitric oxide and the immunomodulation of experimental allergic encephalomyelitis.一氧化氮与实验性变应性脑脊髓炎的免疫调节
Eur J Immunol. 1997 Nov;27(11):2863-9. doi: 10.1002/eji.1830271118.
7
Essential role of TGF-beta in the natural resistance to experimental allergic encephalomyelitis in rats.转化生长因子-β在大鼠实验性变态反应性脑脊髓炎天然抵抗中的重要作用。
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8
Genetic control of the development of experimental allergic encephalomyelitis in rats. Separation of MHC and non-MHC gene effects.大鼠实验性变应性脑脊髓炎发育的遗传控制。主要组织相容性复合体（MHC）基因效应与非MHC基因效应的分离。
J Immunol. 1988 Sep 1;141(5):1489-94.
9
Nitric oxide plays a critical role in the recovery of Lewis rats from experimental autoimmune encephalomyelitis and the maintenance of resistance to reinduction.一氧化氮在实验性自身免疫性脑脊髓炎的Lewis大鼠恢复以及维持对再次诱导的抵抗力方面发挥着关键作用。
J Immunol. 1999 Dec 15;163(12):6841-7.
10
EAE in rat bone marrow chimeras: analysis of the cellular mechanism of BN resistance.大鼠骨髓嵌合体中的实验性自身免疫性脑脊髓炎：BN抗性细胞机制分析
J Immunol. 1981 Apr;126(4):1553-7.

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Nitric oxide enhances Th9 cell differentiation and airway inflammation.一氧化氮增强Th9细胞分化和气道炎症。
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2
GM-CSF-neuroantigen fusion proteins reverse experimental autoimmune encephalomyelitis and mediate tolerogenic activity in adjuvant-primed environments: association with inflammation-dependent, inhibitory antigen presentation.GM-CSF-神经抗原融合蛋白可逆转实验性自身免疫性脑脊髓炎，并在佐剂引发的环境中介导耐受性活性：与炎症依赖性抑制性抗原呈递相关。
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J Neuroinflammation. 2011 Jul 25;8:85. doi: 10.1186/1742-2094-8-85.
8
Regulation of type 17 helper T-cell function by nitric oxide during inflammation.在炎症过程中一氧化氮对 17 型辅助性 T 细胞功能的调节。
Proc Natl Acad Sci U S A. 2011 May 31;108(22):9220-5. doi: 10.1073/pnas.1100667108. Epub 2011 May 16.
9
Nitric oxide and cGMP protein kinase (cGK) regulate dendritic-cell migration toward the lymph-node-directing chemokine CCL19.一氧化氮和环磷酸鸟苷蛋白激酶（cGK）调节树突状细胞向淋巴结趋化因子CCL19的迁移。
Blood. 2006 Feb 15;107(4):1537-45. doi: 10.1182/blood-2005-07-2901. Epub 2005 Oct 25.
10
Nitric oxide and multiple sclerosis.一氧化氮与多发性硬化症
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本文引用的文献

1
Nitric oxide induces polarization of actin in encephalitogenic T cells and inhibits their in vitro trans-endothelial migration in a p70S6 kinase-independent manner.一氧化氮可诱导致脑炎性T细胞中肌动蛋白极化，并以不依赖p70S6激酶的方式抑制其体外跨内皮迁移。
FASEB J. 2003 Jul;17(10):1337-9. doi: 10.1096/fj.02-0577fje. Epub 2003 May 20.
2
Genetic background determines sensitivity to the inhibitory function of NO on T cell proliferation and the amounts of NO production mediated through IFN-gamma.遗传背景决定了对一氧化氮（NO）对T细胞增殖抑制功能的敏感性以及通过γ干扰素介导的NO产生量。
Microbiol Immunol. 2002;46(8):555-63. doi: 10.1111/j.1348-0421.2002.tb02733.x.
3
Cellular and genetic factors involved in the difference between Brown Norway and Lewis rats to develop respectively type-2 and type-1 immune-mediated diseases.参与棕色挪威大鼠和刘易斯大鼠分别易患2型和1型免疫介导疾病差异的细胞和遗传因素。
Immunol Rev. 2001 Dec;184:145-60. doi: 10.1034/j.1600-065x.2001.1840114.x.
4
Macrophages and nitric oxide as the possible cellular and molecular basis for strain and gender differences in susceptibility to autoimmune central nervous system inflammation.巨噬细胞和一氧化氮作为自身免疫性中枢神经系统炎症易感性中品系和性别差异的可能细胞和分子基础。
Immunol Cell Biol. 2002 Apr;80(2):188-97. doi: 10.1046/j.1440-1711.2002.01072.x.
5
The CD8 T cell compartment plays a dominant role in the deficiency of Brown-Norway rats to mount a proper type 1 immune response.在棕色挪威大鼠无法产生适当的1型免疫反应的缺陷中，CD8 T细胞区室起主要作用。
J Immunol. 2002 Jan 1;168(1):162-70. doi: 10.4049/jimmunol.168.1.162.
6
Inhibition of nitric oxide synthase initiates relapsing remitting experimental autoimmune encephalomyelitis in rats, yet nitric oxide appears to be essential for clinical expression of disease.一氧化氮合酶的抑制引发大鼠复发缓解型实验性自身免疫性脑脊髓炎，但一氧化氮似乎对疾病的临床表现至关重要。
J Immunol. 2001 Nov 15;167(10):5904-12. doi: 10.4049/jimmunol.167.10.5904.
7
Gold is a T cell polyclonal activator in BN and LEW rats but favors IL-4 expression only in autoimmune prone BN rats.在BN和LEW大鼠中，金是一种T细胞多克隆激活剂，但仅在自身免疫易感的BN大鼠中促进白细胞介素-4的表达。
Eur J Immunol. 2001 Aug;31(8):2266-76. doi: 10.1002/1521-4141(200108)31:8<2266::aid-immu2266>3.0.co;2-6.
8
Essential role of TGF-beta in the natural resistance to experimental allergic encephalomyelitis in rats.转化生长因子-β在大鼠实验性变态反应性脑脊髓炎天然抵抗中的重要作用。
Eur J Immunol. 2001 Apr;31(4):1132-40.
9
Interleukin-10 is an unequivocal Th2 parameter in the rat, whereas interleukin-4 is not.
Scand J Immunol. 2000 Nov;52(5):519-24. doi: 10.1046/j.1365-3083.2000.00804.x.
10
Heterogeneity of multiple sclerosis lesions: implications for the pathogenesis of demyelination.多发性硬化症病变的异质性：对脱髓鞘发病机制的影响。
Ann Neurol. 2000 Jun;47(6):707-17. doi: 10.1002/1531-8249(200006)47:6<707::aid-ana3>3.0.co;2-q.

一氧化氮有助于棕色挪威大鼠对实验性自身免疫性脑脊髓炎产生抵抗力。

Nitric oxide contributes to resistance of the Brown Norway rat to experimental autoimmune encephalomyelitis.

作者信息

Staykova Maria A, Paridaen Judith T, Cowden William B, Willenborg David O

机构信息

Neurosciences Research Unit, The Canberra Hospital, Canberra, Australia.

出版信息

Am J Pathol. 2005 Jan;166(1):147-57. doi: 10.1016/S0002-9440(10)62240-7.

DOI:10.1016/S0002-9440(10)62240-7
PMID:15632008
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1602296/
Abstract

The Brown Norway (BN) rat is reported to be resistant to the induction of experimental autoimmune encephalomyelitis (EAE) and a number of mechanisms have been suggested to explain this resistance. In work reported here we provide evidence that such resistance in the BN rat can be accounted for, at least in part, by their ability to produce higher levels of nitric oxide (NO) than susceptible strains of rats. Spleen cells from the BN rat make significantly more NO following in vitro stimulation than do cells from the Lewis or PVG rat and following in vivo immunization using complete Freund's adjuvant (CFA) the BN rat makes substantially more NO than either susceptible strain. If carbonyl iron is used as adjuvant in vivo there is no increase in NO levels in the BN rat and they are rendered highly susceptible to EAE. Immunizing with CFA simultaneously with neuroantigen and carbonyl iron drives up NO levels and the resistance is restored. EAE produced using carbonyl iron is characterized by extensive macrophage/microglia presence in the central nervous system lesions of the BN rat yet the cytokine profile in the lymph nodes does not differ from that in the EAE Lewis rats.

摘要

据报道，棕色挪威（BN）大鼠对实验性自身免疫性脑脊髓炎（EAE）的诱导具有抗性，并且已经提出了多种机制来解释这种抗性。在本文报道的研究中，我们提供了证据表明，BN大鼠的这种抗性至少部分可以归因于它们产生比易感大鼠品系更高水平一氧化氮（NO）的能力。与Lewis或PVG大鼠的细胞相比，BN大鼠的脾细胞在体外刺激后产生的NO明显更多，并且在使用完全弗氏佐剂（CFA）进行体内免疫后，BN大鼠产生的NO比任何一种易感品系都要多得多。如果在体内使用羰基铁作为佐剂，BN大鼠的NO水平不会增加，并且它们对EAE变得高度易感。同时用CFA和神经抗原以及羰基铁进行免疫会提高NO水平，并且抗性得以恢复。使用羰基铁诱导产生的EAE的特征是，在BN大鼠的中枢神经系统病变中有大量巨噬细胞/小胶质细胞存在，然而淋巴结中的细胞因子谱与EAE Lewis大鼠的并无差异。