Emerging targets for reprograming the immune response to promote repair and recovery of function after spinal cord injury

被引:57
作者
Brennan, Faith H. [1 ]
Popovich, Phillip G. [1 ]
机构
[1] Ohio State Univ, Wexner Med Ctr, Ctr Brain & Spinal Cord Repair, Dept Neurosci, 694 Biomedical Res Tower,460 W 12th Ave, Columbus, OH 43201 USA
关键词
antigen presentation; intestinal dysbiosis; macrophage polarization; microRNA; neurodegeneration; CHONDROITINASE ABC PROMOTES; MYELIN BASIC-PROTEIN; INFLAMMATORY RESPONSE; CELLS PROTECT; T-CELLS; MACROPHAGE ACTIVATION; RECEPTOR ANTAGONIST; NEURITE OUTGROWTH; SECONDARY INJURY; DENDRITIC CELLS;
D O I
10.1097/WCO.0000000000000550
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Purpose of review In adult mammals, a traumatic spinal cord injury (SCI) elicits a chronic unregulated neuroinflammatory response accompanied by seemingly paradoxical suppression of systemic immunity. These SCI-induced changes in immune function contribute to poor neurological outcomes and enhanced morbidity or mortality. Nonspecific anti-inflammatory or proinflammatory therapies are ineffective and can even worsen outcomes. Therefore, recent experimental SCI research has advanced the understanding of how neuroimmune crosstalk contributes to spinal cord and systemic pathology. Recent findings It is now appreciated that the immune response caused by injury to the brain or spinal cord encompasses heterogeneous elements that can drive events on the spectrum between exacerbating pathology and promoting tissue repair, within the spinal cord and throughout the body. Recent novel discoveries regarding the role and regulation of soluble factors, monocytes/macrophages, microRNAs, lymphocytes and systemic immune function are highlighted in this review. Summary A more nuanced understanding of how the immune system responds and reacts to nervous system injury will present an array of novel therapeutic opportunities for clinical SCI and other forms of neurotrauma.
引用
收藏
页码:334 / 344
页数:11
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