Article ID Journal Published Year Pages File Type
3065746 Journal of Neuroimmunology 2007 13 Pages PDF
Abstract

The inflammatory wound healing response of the central nervous system (CNS) following mechanical injury is characterized by at least one or two phases of T cell infiltration. Surprisingly, whether T cells play a beneficial or detrimental role in these processes is still controversial. It has been suggested that autoimmune T cells may provide “protective autoimmunity”, however, after CNS injury, injections of autoimmune T cells and vaccine strategies led to both improvement in some models and exacerbation of the damage in others. Here, we review increasing evidence that a specific T cell subpopulation, namely T helper cells type 2 (Th2 cells) are particularly beneficial in the context of CNS lesions. CNS injuries such as mechanical lesions or stroke induce a systemic immunosuppression, which is characterized by a systemic shift towards a Th2 cytokine pattern. Simplified, this systemic Th2 shift results in reduced cell-mediated immune responses, and, to a lesser extent, humoral immune responses. Furthermore, treatment with potent Th2 inducers such as glatiramer acetate or statins, as well as vaccination strategies using Th2-inducing adjuvants for immunization such as aluminum hydroxide, result in increased neuroprotection and regeneration — without development of autoimmune CNS inflammation. Thus, it is tempting to speculate that a systemic Th2 shift is part of a necessary CNS wound healing response after injury, by furthering regeneration and preventing autoimmune disease of the CNS. Within this context, investigating the potential of a systemic Th2 shift to improve outcome after CNS injury, including the control of possible side-effects such as increased susceptibility to infection and allergic responses, is extremely promising.

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