The paradox of chronic neuroinflammation, systemic immune suppression, autoimmunity after traumatic chronic spinal cord injury.
The paradox of chronic neuroinflammation, systemic immune suppression, autoimmunity after traumatic chronic spinal cord injury.
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DOI：
10.1016/j.expneurol.2014.04.023
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发表时间：
2014-08
影响因子：
5.3
通讯作者：
Popovich, Phillip G.
中科院分区：
文献类型：
--
作者：
Schwab, Jan M.;Zhang, Yi;Kopp, Marcel A.;Brommer, Benedikt;Popovich, Phillip G.
在脊髓损伤（SCI）后从急性到慢性恢复阶段的过渡过程中，免疫功能障碍的状态不断演变，加剧了与临床上更明显的神经功能缺损相关的问题。由于损伤直接影响嵌入脊髓的“免疫特权/特化”环境中的细胞，因此可能发生适应不良或低效反应。总的来说，这些反应符合“SCI疾病”连续体的一部分，并且是改善神经修复和神经学结果的重要治疗靶点。通用免疫抑制疗法在很大程度上是不成功的，主要是因为炎症和免疫发挥有益的（可塑性增强）和有害的（例如神经胶质和神经变性;继发性损伤）作用，这些功能随时间变化。此外，“区室化”研究仅限于脊髓内炎症和相关的细胞或分子变化，忽视了CNS的结构和功能受到全身免疫挑战的影响以及免疫系统与神经系统的硬连线。在这里，我们考虑从急性到慢性SCI的进展过程中的相互作用。具体来说，我们调查受损/非解决椎管内炎症和悖论的全身炎症反应，在面对持续的慢性免疫抑制和自身免疫。全身炎症反应综合征（SIRS），代偿性抗炎反应综合征（汽车）和“神经源性”脊髓损伤诱导的免疫抑制综合征（SCI-IDS）的概念进行了讨论，作为受损的“宿主防御”和创伤诱导的自身免疫的决定因素。
During the transition from acute to chronic stages of recovery after spinal cord injury (SCI), there is an evolving state of immunologic dysfunction that exacerbates the problems associated with the more clinically obvious neurologic deficits. Since injury directly affects cells embedded within the “immune privileged/specialized” milieu of the spinal cord, maladaptive or inefficient responses are likely to occur. Collectively, these responses qualify as part of the continuum of “SCI disease” and are important therapeutic targets to improve neural repair and neurological outcome. Generic immune suppressive therapies have been largely unsuccessful, mostly because nflammation and immunity exert both beneficial (plasticity enhancing) and detrimental (e.g. glia- and neurodegenerative; secondary damage) effects and these functions change over time. Moreover, “compartmentalized” investigations, limited to only intraspinal inflammation and associated cellular or molecular changes in the spinal cord, neglect the reality that the structure and function of the CNS is influenced by systemic immune challenges and that the immune system is hardwired into the nervous system. Here, we consider this interplay during the progression from acute to chronic SCI. Specifically, we survey impaired/non-resolving intraspinal inflammation and the paradox of systemic inflammatory responses in the face of ongoing chronic immune suppression and autoimmunity. The concepts of systemic inflammatory response syndrome (SIRS), compensatory anti-inflammatory response syndrome (CARS) and ‘neurogenic’ spinal cord injury-induced immune depression syndrome (SCI-IDS) are discussed as determinants of impaired ‘host-defense’ and trauma-induced autoimmunity.
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DOI：
10.1093/brain/awr074
发表时间：
2011-05
期刊：
Brain : a journal of neurology
影响因子：
--
作者：
Beers DR;Henkel JS;Zhao W;Wang J;Huang A;Wen S;Liao B;Appel SH
通讯作者：
Appel SH
影响因子：
--
作者：
DEVIVO, MJ;KARTUS, PL;FINE, PR
通讯作者：
FINE, PR
影响因子：
6
作者：
Bradl, M;Bauer, J;Lassmann, H
通讯作者：
Lassmann, H
影响因子：
5
作者：
CRUSE, JM;LEWIS, RE;BRITT, R
通讯作者：
BRITT, R
影响因子：
16.8
作者：
Ankeny DP;Popovich PG
通讯作者：
Popovich PG