title: The role of T helper cells in neuroprotection and regeneration.
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.
authors.affiliation: Institute of Cell Biology and Neurobiology, Center for Anatomy, Charité -- Universitätsmedizin Berlin, Charitépl. 1, D-10098 Berlin, Germany. sven.hendrix@charite.de
authors.forename: Sven
authors.initials: S
authors.lastname: Hendrix
authors.forename: Robert
authors.initials: R
authors.lastname: Nitsch
mesh_terms: D000818:Animals; D002493:Central Nervous System Diseases / Q000150:complications / Q000473:pathology*; D006801:Humans; D009410:Nerve Degeneration / Q000209:etiology / Q000517:prevention & control*; D012038:Regeneration / Q000502:physiology*; D018418:Th2 Cells / Q000502:physiology*; D014945:Wound Healing / Q000502:physiology