Infection with Mycobacterium bovis BCG Diverts Traffic of Myelin Oligodendroglial Glycoprotein Autoantigen-Specific T Cells Away from the Central Nervous System and Ameliorates Experimental Autoimmune Encephalomyelitis

Diane L. Sewell; Emily K. Reinke; Dominic O. Co; Laura H. Hogan; Robert B. Fritz; Matyas Sandor

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Infection with Mycobacterium bovis BCG Diverts Traffic of Myelin Oligodendroglial Glycoprotein Autoantigen-Specific T Cells Away from the Central Nervous System and Ameliorates Experimental Autoimmune Encephalomyelitis

机译：牛分枝杆菌BCG感染可转移远离中枢神经系统的髓鞘少突胶质糖蛋白自身抗原特异性T细胞的运输，并减轻实验性自身免疫性脑脊髓炎

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Infectious agents have been proposed to influence susceptibility to autoimmune diseases such as multiple sclerosis. We induced a Th1-mediated central nervous system (CNS) autoimmune disease, experimental autoimmune encephalomyelitis (EAE) in mice with an ongoing infection with Mycobacterium bovis strain bacillus Calmette-Guérin (BCG) to study this possibility. C57BL/6 mice infected with live BCG for 6 weeks were immunized with myelin oligodendroglial glycoprotein peptide (MOG_35-55) to induce EAE. The clinical severity of EAE was reduced in BCG-infected mice in a BCG dose-dependent manner. Inflammatory-cell infiltration and demyelination of the spinal cord were significantly lessened in BCG-infected animals compared with uninfected EAE controls. ELISPOT and gamma interferon intracellular cytokine analysis of the frequency of antigen-specific CD4+ T cells in the CNS and in BCG-induced granulomas and adoptive transfer of MOG_35-55-specific green fluorescent protein-expressing cells into BCG-infected animals indicated that nervous tissue-specific (MOG_35-55) CD4+ T cells accumulate in the BCG-induced granuloma sites. These data suggest a novel mechanism for infection-mediated modulation of autoimmunity. We demonstrate that redirected trafficking of activated CNS antigen-specific CD4+ T cells to local inflammatory sites induced by BCG infection modulates the initiation and progression of a Th1-mediated CNS autoimmune disease.

机译：已经提出了感染因子来影响对自身免疫疾病如多发性硬化的易感性。我们在持续感染牛分枝杆菌杆菌卡介特-桂林（BCG）的小鼠中诱导了Th1介导的中枢神经系统（CNS）自身免疫性疾病，实验性自身免疫性脑脊髓炎（EAE），以研究这种可能性。用髓鞘少突胶质糖蛋白肽（MOG _{35-55 ）免疫活BCG感染6周的C57BL / 6小鼠，以诱导EAE。在BCG感染的小鼠中，EAE的临床严重程度以BCG剂量依赖性方式降低。与未感染的EAE对照相比，在BCG感染的动物中，脊髓的炎性细胞浸润和脱髓鞘明显减少。 ELISPOT和γ干扰素细胞内细胞因子分析中枢神经系统和BCG诱导的肉芽肿中抗原特异性CD4 + T细胞的频率以及MOG _{35-55 -的过继转移特定的绿色荧光蛋白表达细胞进入被BCG感染的动物，表明神经组织特异性（MOG _{35-55 ）CD4 + T细胞积聚在BCG诱导的肉芽肿部位。这些数据表明感染介导的自身免疫调节的新机制。我们证明了激活的CNS抗原特异性CD4 + T细胞向由BCG感染诱导的局部炎症位点的重定向贩运可调节Th1介导的CNS自身免疫病的发生和发展。}}} 展开▼

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《Clinical and diagnostic laboratory immunology》 |2003年第4期|共9页

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Diane L. Sewell; Emily K. Reinke; Dominic O. Co; Laura H. Hogan; Robert B. Fritz; Matyas Sandor;
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专利

1. MHC Class II-Regulated Central Nervous System Autoaggression and T Cell Responses in Peripheral Lymphoid Tissues Are Dissociated in Myelin Oligodendrocyte Glycoprotein-Induced Experimental Autoimmune Encephalomyelitis [J] . Robert Weissert, Katrien L. de Graaf, Maria K. Storch, The Journal of Immunology: Official Journal of the American Association of Immunologists . 2001,第12期

机译：MHC II类调节的中枢神经系统自发攻击和外周淋巴组织中的T细胞反应在髓鞘少突胶质糖蛋白诱导的实验性自身免疫性脑脊髓炎中解离

2. MHC Class II-Regulated Central Nervous System Autoaggression and T Cell Responses in Peripheral Lymphoid Tissues Are Dissociated in Myelin Oligodendrocyte Glycoprotein-Induced Experimental Autoimmune Encephalomyelitis [J] . Robert Weissert, Katrien L. de Graaf, Maria K. Storch, The journal of immunology . 2001,第12期

机译：MHC II类调节的中枢神经系统自发攻击和外周淋巴组织中的T细胞反应在髓鞘少突胶质糖蛋白诱导的实验性自身免疫性脑脊髓炎中解离

3. Kinetics and cellular origin of cytokines in the central nervous system: insight into mechanisms of myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis. [J] . Juedes AE, Hjelmstrom P, Bergman CM, The Journal of Immunology: Official Journal of the American Association of Immunologists . 2000,第1期

机译：中枢神经系统细胞因子的动力学和细胞起源：髓鞘少突胶质细胞糖蛋白诱导的实验性自身免疫性脑脊髓炎的机制的见解。

4. Rotating Magnetic Field Ameliorates Experimental Autoimmune Encephalomyelitis by Promoting T cell Peripheral Accumulation and Regulating the Balance of Treg and TH1/TH17 [C] . Tianying Zhan, Xiaomei Wang, Zijun Ouyang, The 8th International Conference on Magneto- Science（第八届国际磁科学会议）论文集 . -1

机译：旋转磁场通过促进T细胞周围积累和调节Treg和Th1 / Th17的平衡来改善实验性自身免疫性脑炎。

5. Macrophage migration inhibitory factor: A study of the effects on the central nervous system microenvironment in experimental autoimmune encephalomyelitis. [D] . Cox, Gina Mavrikis. 2011

机译：巨噬细胞迁移抑制因子：对实验性自身免疫性脑脊髓炎对中枢神经系统微环境影响的研究。

6. Infection with Mycobacterium bovis BCG Diverts Traffic of Myelin Oligodendroglial Glycoprotein Autoantigen-Specific T Cells Away from the Central Nervous System and Ameliorates Experimental Autoimmune Encephalomyelitis [O] . Diane L. Sewell, Emily K. Reinke, Dominic O. Co, 2003

机译：牛分枝杆菌BCG感染可转移远离中枢神经系统的髓磷脂少突胶质糖蛋白自身抗原特异性T细胞的运输并减轻实验性自身免疫性脑脊髓炎

7. Infection with Mycobacterium bovis BCG Diverts Traffic of Myelin Oligodendroglial Glycoprotein Autoantigen-Specific T Cells Away from the Central Nervous System and Ameliorates Experimental Autoimmune Encephalomyelitis [O] . Sewell, Diane L., Reinke, Emily K., Co, Dominic O., 2003

机译：牛分枝杆菌卡介苗的感染转移了远离中枢神经系统的髓磷脂少突胶质糖蛋白糖原自身抗原特异性T细胞的运输，并减轻了实验性自身免疫性脑脊髓炎

1. C57BL/6小鼠性别差异对髓鞘少突胶质糖蛋白诱导的实验性自身脑脊髓炎疾病的影响 [J] . 王婷婷 ,杜昌升 . 生物化学与生物物理进展 . 2013,第011期

1. compound or a pharmaceutically acceptable salt, solvate or hydrate thereof, pharmaceutical composition, and, methods to inhibit angiogenesis, to inhibit or reduce the polymerization of tubulin or the stability of tubulin in a cell, to inhibit pde4 activity in a cell , to inhibit tumor necrosis factor-alpha (tnf-alpha) activity in a cell, to treat or ameliorate an inflammatory disorder, to treat or ameliorate cancer, to inhibit cancer cell proliferation, to mark, block or destroy tumor vasculature function, to mark, block or destroy tumor vessel endothelium, to mark, block or destroy tumor vasculature function and inhibit angiogenesis in a tumor and to treat or ameliorate a central nervous system disorder [P] . 外国专利： BRPI0514857A . 2008-05-06

机译：化合物或其药学上可接受的盐，溶剂化物或水合物，药物组合物以及抑制血管生成，抑制或降低微管蛋白聚合或微管蛋白稳定性的方法，抑制细胞中pde4活性，抑制肿瘤的方法细胞中的坏死因子-α（tnf-alpha）活性，用于治疗或改善炎症性疾病，治疗或改善癌症，抑制癌细胞增殖，标记，阻断或破坏肿瘤血管功能，标记，阻断或破坏肿瘤血管内皮，标记，阻断或破坏肿瘤的脉管系统功能并抑制肿瘤中的血管生成，并治疗或改善中枢神经系统疾病

2. compound or a pharmaceutically acceptable salt, solvate or hydrate thereof, pharmaceutical composition, and methods for inhibiting angiogenesis, for inhibiting or reducing tubulin polymerization or tubulin stability in a cell, for inhibiting pde4 activity in a cell , to inhibit tumor necrosis factor-alpha (tnf-alpha) activity in a cell, to treat or ameliorate an inflammatory disorder, to treat or ameliorate cancer, to inhibit cancer cell proliferation, to mark, block or destroy Tumor vasculature function, to tag, block or destroy tumor vessel endothelium, to tag, block or destroy tumor vasculature function and inhibit angiogenesis in a tumor, and to treat or ameliorate a central nervous system disorder [P] . 外国专利： BRPI0514890A . 2007-11-27

机译：化合物或其药学上可接受的盐，溶剂化物或水合物，药物组合物以及抑制血管生成，抑制或降低细胞微管蛋白聚合或微管蛋白稳定性，抑制细胞中pde4活性，抑制肿瘤坏死因子-α（细胞中的tnf-alpha）活性，以治疗或改善炎症性疾病，以治疗或改善癌症，抑制癌细胞的增殖，标记，阻断或破坏肿瘤血管功能，标记，阻断或破坏肿瘤血管内皮，标记，阻断或破坏肿瘤血管系统功能并抑制肿瘤中的血管生成，并治疗或改善中枢神经系统疾病

3. Use of a non-laboratory virus strain, methods for determining whether a gene has an effect on a phenotype associated with a peripheral and central nervous system disorder or on a peripheral and central nervous system cell to determine whether a gene encodes an antigen associated with a pathogenic infection or cancer, to determine the suitability of a non-laboratory virus strain for modification to a modified strain, to determine whether a gene enhances the anti-tumor effects of a virus, and to produce an oncolytic non-laboratory virus strain. , modified, non-laboratory virus strain, use of a gene, hsv1 js1 strain, pharmaceutical composition, and, methods for treating a tumor in an individual, supplying a gene to an individual and treating or preventing a disorder of the peripheral nervous systems and central [P] . 外国专利： BR0107736A . 2002-11-19

机译：使用非实验室病毒株，确定基因是否对与周围和中枢神经系统疾病有关的表型或对周围和中枢神经系统细胞有影响的方法，以确定基因是否编码与肝炎相关的抗原致病性感染或癌症，以确定非实验室病毒株对修饰菌株的适应性，确定基因是否增强病毒的抗肿瘤作用，并产生溶瘤性非实验室病毒株。，修饰的非实验室病毒株，基因的用途，hsv1 js1株，药物组合物以及治疗个体肿瘤，向个体提供基因并治疗或预防周围神经系统疾病的方法中央

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Infection with Mycobacterium bovis BCG Diverts Traffic of Myelin Oligodendroglial Glycoprotein Autoantigen-Specific T Cells Away from the Central Nervous System and Ameliorates Experimental Autoimmune Encephalomyelitis

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