Following an injury to the central nervous system (CNS), spontaneous plasticity is observed throughout the neuraxis and affects multiple key circuits. Much of this spontaneous plasticity can elicit beneficial and deleterious functional outcomes, depending on the context of plasticity and circuit affected. Injury-induced activation of the neuroimmune system has been proposed to be a major factor in driving this plasticity, as neuroimmune and inflammatory factors have been shown to influence cellular, synaptic, structural, and anatomical plasticity. Here, we will review the mechanisms through which the neuroimmune system mediates plasticity after CNS injury. Understanding the role of specific neuroimmune factors in driving adaptive and maladaptive plasticity may offer valuable therapeutic insight into how to promote adaptive plasticity and/or diminish maladaptive plasticity, respectively.

中枢神经系统（CNS）受到损伤后，在整个神经轴上都观察到自发可塑性，并影响多个关键回路。这种自发的可塑性大部分可以带来有益的和有害的功能结果，取决于可塑性和受影响回路的情况。已提出损伤诱导的神经免疫系统的激活是驱动这种可塑性的主要因素，因为神经免疫和炎性因子已显示影响细胞，突触，结构和解剖学的可塑性。在这里，我们将回顾中枢神经系统损伤后神经免疫系统介导可塑性的机制。理解特定的神经免疫因子在驱动适应性和适应不良可塑性中的作用可能为如何分别提高适应性可塑性和/或减少适应不良性可塑性提供有价值的治疗见解。