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RESEARCH PRODUCT

Regeneration After CNS Lesion: Help from the Immune System?

subject

description

Traumatic injury to the central nervous system (CNS) is followed by an inflammatory response, which is characterized by at least two very distinct phases: First, a short highly controlled burst of acute inflammatory defense and second, a long-term remodeling phase. Similarly, at least one or two phases of T-cell infiltration have been described in CNS trauma models suggesting differential functions of T cells in the acute and remodeling phase. Thus, the role of T cells in CNS trauma is still controversial. Interestingly, vaccine strategies and injections of autoimmune T cells led to both exacerbation of CNS damage after trauma in some models and improvement in others. Here, we suggest that specific subtypes of T cells may be responsible for either the respective beneficial or detrimental effects in the biphasic response of the CNS to trauma. There is increasing evidence that specific subtypes of T cells, in particular T-helper cells type 2 (Th2 cells), may play a beneficial role in the context of CNS lesions by promoting axon outgrowth and – at the same time – protecting from self-reactive CNS inflammation. CNS injury-induced systemic immunosuppression results in a systemic shift toward a Th2 cytokine pattern, which impairs cellular immune responses suggesting a protective function against autoimmunity. Treatment with potent inducers of a Th2 switch such as glatiramer acetate or statins, as well as vaccination strategies using Th2-inducing adjuvants for immunization results in increased neuroprotection and regeneration. However, a systematic analysis of effects of the different T-helper cell subpopulations in the acute and chronic phases after CNS trauma is still desperately needed to develop concepts to explain contradictory findings about beneficial or detrimental T-cell effects in CNS injury and repair.