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本文引用的文献

1
Oestrogen modulates experimental autoimmune encephalomyelitis and interleukin-17 production via programmed death 1.雌激素通过程序性死亡1调节实验性自身免疫性脑脊髓炎和白细胞介素-17的产生。
Immunology. 2009 Mar;126(3):329-35. doi: 10.1111/j.1365-2567.2008.03051.x.
2
Membrane estrogen receptor regulates experimental autoimmune encephalomyelitis through up-regulation of programmed death 1.膜雌激素受体通过上调程序性死亡蛋白1来调节实验性自身免疫性脑脊髓炎。
J Immunol. 2009 Mar 1;182(5):3294-303. doi: 10.4049/jimmunol.0803205.
3
Effect of natalizumab on clinical and radiological disease activity in multiple sclerosis: a retrospective analysis of the Natalizumab Safety and Efficacy in Relapsing-Remitting Multiple Sclerosis (AFFIRM) study.那他珠单抗对多发性硬化症临床及影像学疾病活动的影响:复发缓解型多发性硬化症那他珠单抗安全性与疗效(AFFIRM)研究的回顾性分析
Lancet Neurol. 2009 Mar;8(3):254-60. doi: 10.1016/S1474-4422(09)70021-3. Epub 2009 Feb 7.
4
Beta1 integrins differentially control extravasation of inflammatory cell subsets into the CNS during autoimmunity.β1整合素在自身免疫过程中对炎症细胞亚群渗入中枢神经系统具有不同的调控作用。
Proc Natl Acad Sci U S A. 2009 Feb 10;106(6):1920-5. doi: 10.1073/pnas.0808909106. Epub 2009 Jan 28.
5
Changes in matrix metalloproteinases and their inhibitors during interferon-beta treatment in multiple sclerosis.多发性硬化症患者在β-干扰素治疗期间基质金属蛋白酶及其抑制剂的变化
Clin Immunol. 2009 Feb;130(2):145-50. doi: 10.1016/j.clim.2008.09.010. Epub 2008 Oct 21.
6
IL-23 promotes maintenance but not commitment to the Th17 lineage.白细胞介素-23促进Th17细胞系的维持,但不促进其分化。
J Immunol. 2008 Nov 1;181(9):5948-55. doi: 10.4049/jimmunol.181.9.5948.
7
Beta interferon restricts the inflammatory potential of CD4+ cells through the boost of the Th2 phenotype, the inhibition of Th17 response and the prevalence of naturally occurring T regulatory cells.β干扰素通过增强Th2表型、抑制Th17反应以及使自然产生的调节性T细胞占优势来限制CD4+细胞的炎症潜能。
Mol Immunol. 2008 Sep;45(15):4008-19. doi: 10.1016/j.molimm.2008.06.006. Epub 2008 Jul 18.
8
Engagement of the type I interferon receptor on dendritic cells inhibits T helper 17 cell development: role of intracellular osteopontin.树突状细胞上I型干扰素受体的激活抑制辅助性T细胞17的发育:细胞内骨桥蛋白的作用
Immunity. 2008 Jul 18;29(1):68-78. doi: 10.1016/j.immuni.2008.05.008.
9
Type 1 interferons cool the inflamed brain.1型干扰素使发炎的大脑降温。
Immunity. 2008 May;28(5):600-2. doi: 10.1016/j.immuni.2008.04.006.
10
Distinct and nonredundant in vivo functions of IFNAR on myeloid cells limit autoimmunity in the central nervous system.IFNAR在髓样细胞上独特且非冗余的体内功能限制了中枢神经系统中的自身免疫。
Immunity. 2008 May;28(5):675-86. doi: 10.1016/j.immuni.2008.03.011.

在实验性自身免疫性脑脊髓炎中,抗炎和神经保护药物联合治疗的附加效应。

Additive effects of combination treatment with anti-inflammatory and neuroprotective agents in experimental autoimmune encephalomyelitis.

机构信息

University of California, Los Angeles, Department of Neurology, UCLA Multiple Sclerosis Program, 635 Charles E Young Drive South, Neuroscience Research Building 1, Room 479, Los Angeles, CA 90095, United States.

出版信息

J Neuroimmunol. 2010 Feb 26;219(1-2):64-74. doi: 10.1016/j.jneuroim.2009.11.018. Epub 2009 Dec 14.

DOI:10.1016/j.jneuroim.2009.11.018
PMID:20006910
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3037186/
Abstract

We studied the effects of combination treatment with an anti-inflammatory agent, interferon (IFN)-beta, and a putative neuroprotective agent, an estrogen receptor (ER)-beta ligand, during EAE. Combination treatment significantly attenuated EAE disease severity, preserved axonal densities in spinal cord, and reduced CNS inflammation. Combining ERbeta treatment with IFNbeta reduced IL-17, while it abrogated IFNbeta-mediated increases in Th1 and Th2 cytokines from splenocytes. Additionally, combination treatment reduced VLA-4 expression on CD4+ T cells, while it abrogated IFNbeta-mediated decreases in MMP-9. Our data demonstrate that combination treatments can result in complex effects that could not have been predicted based on monotherapy data alone.

摘要

我们研究了在 EAE 期间联合使用抗炎药干扰素 (IFN)-β和一种假定的神经保护剂雌激素受体 (ER)-β配体的治疗效果。联合治疗显著减轻了 EAE 的严重程度,保留了脊髓中的轴突密度,并减少了中枢神经系统的炎症。将 ERβ治疗与 IFNβ 联合使用可减少 IL-17,同时消除了 IFNβ 介导的脾细胞 Th1 和 Th2 细胞因子的增加。此外,联合治疗降低了 CD4+T 细胞上的 VLA-4 表达,同时消除了 IFNβ 介导的 MMP-9 减少。我们的数据表明,联合治疗可能会产生复杂的效果,这些效果不能仅根据单药治疗数据来预测。