• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

外周免疫对神经病理性疼痛相关中枢神经胶质激活的维持作用。

Peripheral immune contributions to the maintenance of central glial activation underlying neuropathic pain.

机构信息

Discipline of Pharmacology, School of Medical Sciences, University of Adelaide, Adelaide, SA 5005, Australia.

出版信息

Brain Behav Immun. 2011 Oct;25(7):1322-32. doi: 10.1016/j.bbi.2011.04.003. Epub 2011 Apr 7.

DOI:10.1016/j.bbi.2011.04.003
PMID:21496480
Abstract

Recent evidence implicates an adaptive immune response in the central nervous system (CNS) mechanisms of neuropathic pain. This review identifies how neuropathic pain alters CNS immune privilege to facilitate T cell infiltration. Once in the CNS, T cells may interact with the local antigen presenting cells, microglia, via the major histocompatibility complex and the costimulatory molecules CD40 and B7. In this way, T cells may contribute to the maintenance of neuropathic pain through pro-inflammatory interactions with microglia and by facilitating the activation of astrocytes in the spinal dorsal horn. Based on the evidence presented in this review, we suggest that this bidirectional, pro-inflammatory system of neurons, glia and T cells in neuropathic pain should be renamed the pentapartite synapse, and identifies the latest member as a potential disease-modifying therapeutic target.

摘要

最近的证据表明,适应性免疫反应参与了中枢神经系统(CNS)神经性疼痛的机制。本综述确定了神经性疼痛如何改变 CNS 免疫特权以促进 T 细胞浸润。一旦进入中枢神经系统,T 细胞可能通过主要组织相容性复合体和共刺激分子 CD40 和 B7 与局部抗原呈递细胞小胶质细胞相互作用。通过这种方式,T 细胞可能通过与小胶质细胞的促炎相互作用以及促进脊髓背角星形胶质细胞的激活,有助于维持神经性疼痛。基于本综述中提出的证据,我们建议将神经性疼痛中神经元、神经胶质和 T 细胞的这种双向促炎系统重新命名为五重突触,并将最新成员确定为潜在的疾病修饰治疗靶点。

相似文献

1
Peripheral immune contributions to the maintenance of central glial activation underlying neuropathic pain.外周免疫对神经病理性疼痛相关中枢神经胶质激活的维持作用。
Brain Behav Immun. 2011 Oct;25(7):1322-32. doi: 10.1016/j.bbi.2011.04.003. Epub 2011 Apr 7.
2
Immune and inflammatory mechanisms in neuropathic pain.神经病理性疼痛中的免疫和炎症机制。
Brain Res Rev. 2006 Aug;51(2):240-64. doi: 10.1016/j.brainresrev.2005.11.004. Epub 2006 Jan 4.
3
The role of glia and the immune system in the development and maintenance of neuropathic pain.胶质细胞和免疫系统在神经性疼痛的发生和维持中的作用。
Pain Pract. 2010 May-Jun;10(3):167-84. doi: 10.1111/j.1533-2500.2010.00367.x. Epub 2010 Apr 5.
4
Importance of glial activation in neuropathic pain.胶质细胞激活在神经病理性疼痛中的重要性。
Eur J Pharmacol. 2013 Sep 15;716(1-3):106-19. doi: 10.1016/j.ejphar.2013.01.072. Epub 2013 Mar 13.
5
Involvement of inflammatory mediators in neuropathic pain caused by vincristine.炎症介质在长春新碱所致神经性疼痛中的作用
Int Rev Neurobiol. 2009;85:179-90. doi: 10.1016/S0074-7742(09)85014-9.
6
Distribution of the immune inhibitory molecules CD200 and CD200R in the normal central nervous system and multiple sclerosis lesions suggests neuron-glia and glia-glia interactions.免疫抑制分子CD200和CD200R在正常中枢神经系统和多发性硬化病变中的分布提示神经元-胶质细胞和胶质细胞-胶质细胞之间的相互作用。
J Neuropathol Exp Neurol. 2009 Feb;68(2):159-67. doi: 10.1097/NEN.0b013e3181964113.
7
The neuropathic pain triad: neurons, immune cells and glia.神经病理性疼痛三联征:神经元、免疫细胞和神经胶质细胞。
Nat Neurosci. 2007 Nov;10(11):1361-8. doi: 10.1038/nn1992.
8
Pathophysiology of peripheral neuropathic pain: immune cells and molecules.外周神经性疼痛的病理生理学:免疫细胞与分子
Anesth Analg. 2007 Sep;105(3):838-47. doi: 10.1213/01.ane.0000275190.42912.37.
9
Immune responses of microglia in the spinal cord: contribution to pain states.脊髓中小胶质细胞的免疫反应:对疼痛状态的贡献。
Exp Neurol. 2012 Apr;234(2):262-70. doi: 10.1016/j.expneurol.2011.12.021. Epub 2011 Dec 27.
10
Induction of primary T cell responses by human glial cells.人神经胶质细胞对原发性T细胞反应的诱导作用。
J Neurosci Res. 1993 Nov 1;36(4):382-90. doi: 10.1002/jnr.490360404.

引用本文的文献

1
Provoked cytokine response is not associated with distress or induced secondary hyperalgesia in people with suppressed HIV.激发的细胞因子反应与HIV抑制人群的痛苦或诱发的继发性痛觉过敏无关。
medRxiv. 2025 Mar 11:2025.01.21.25320673. doi: 10.1101/2025.01.21.25320673.
2
The contribution of clock genes BMAL1 and PER2 in osteoarthritis-associated pain.生物钟基因BMAL1和PER2在骨关节炎相关性疼痛中的作用。
Neurobiol Pain. 2024 Dec 22;17:100177. doi: 10.1016/j.ynpai.2024.100177. eCollection 2025 Jan-Jun.
3
Minocycline Abrogates Individual Differences in Nerve Injury-Evoked Affective Disturbances in Male Rats and Prevents Associated Supraspinal Neuroinflammation.
米诺环素消除了雄性大鼠神经损伤诱发的情感障碍的个体差异,并预防了相关的中枢神经炎症。
J Neuroimmune Pharmacol. 2024 Jun 15;19(1):30. doi: 10.1007/s11481-024-10132-y.
4
Increased risk of persistent neuropathic pain after traumatic nerve injury and surgery for carriers of a human leukocyte antigen haplotype.携带人类白细胞抗原单倍型的患者在创伤性神经损伤和手术后,持续神经性疼痛的风险增加。
Pain. 2024 Jun 1;165(6):1404-1412. doi: 10.1097/j.pain.0000000000003143. Epub 2023 Dec 22.
5
Morphine aggravates inflammatory, behavioral, and hippocampal structural deficits in septic rats.吗啡加重脓毒症大鼠的炎症、行为和海马结构缺陷。
Sci Rep. 2023 Dec 5;13(1):21460. doi: 10.1038/s41598-023-46427-y.
6
Study protocol: an observational study of distress, immune function and persistent pain in HIV.研究方案:一项关于 HIV 患者痛苦、免疫功能和持续性疼痛的观察性研究。
BMJ Open. 2022 Jun 3;12(6):e059723. doi: 10.1136/bmjopen-2021-059723.
7
The Neuroimmune Interface and Chronic Pain Through the Lens of Production Animals.从生产动物视角看神经免疫界面与慢性疼痛
Front Neurosci. 2022 May 19;16:887042. doi: 10.3389/fnins.2022.887042. eCollection 2022.
8
Mechanistic Insight into the Effects of Curcumin on Neuroinflammation-Driven Chronic Pain.姜黄素对神经炎症驱动的慢性疼痛影响的机制洞察。
Pharmaceuticals (Basel). 2021 Aug 7;14(8):777. doi: 10.3390/ph14080777.
9
Sanguinarine Attenuates Neuropathic Pain in a Rat Model of Chronic Constriction Injury.血根碱减轻慢性缩窄性损伤大鼠模型的神经病理性疼痛。
Biomed Res Int. 2021 Apr 21;2021:3689829. doi: 10.1155/2021/3689829. eCollection 2021.
10
Role of innate immunity in chemotherapy-induced peripheral neuropathy.先天免疫在化疗诱导的周围神经病中的作用。
Neurosci Lett. 2021 Jun 11;755:135941. doi: 10.1016/j.neulet.2021.135941. Epub 2021 May 4.