作者: Sven Hendrix , Robert Nitsch
DOI: 10.1007/978-1-4419-1676-1_11
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摘要: Traumatic injury to the central nervous system (CNS) is followed by an inflammatory response, which characterized at least two very distinct phases: First, a short highly controlled burst of acute defense and second, long-term remodeling phase. Similarly, one or phases T-cell infiltration have been described in CNS trauma models suggesting differential functions T cells Thus, role still controversial. Interestingly, vaccine strategies injections autoimmune led both exacerbation damage after some improvement others. Here, we suggest that specific subtypes may be responsible for either respective beneficial detrimental effects biphasic response trauma. There increasing evidence cells, particular T-helper type 2 (Th2 cells), play context lesions promoting axon outgrowth – same time protecting from self-reactive inflammation. injury-induced systemic immunosuppression results shift toward Th2 cytokine pattern, impairs cellular immune responses protective function against autoimmunity. Treatment with potent inducers switch such as glatiramer acetate statins, well vaccination using Th2-inducing adjuvants immunization increased neuroprotection regeneration. However, systematic analysis different cell subpopulations chronic desperately needed develop concepts explain contradictory findings about repair.