title: γδ T cells as early sensors of tissue damage and mediators of secondary neurodegeneration.
abstract: Spontaneous or medically induced reperfusion occurs in up to 70% of patients within 24 h after cerebral ischemia. Reperfusion of ischemic brain tissue can augment the inflammatory response that causes additional injury. Recently, T cells have been shown to be an essential part of the post-ischemic tissue damage, and especially IL-17 secreting T cells have been implicated in the pathogenesis of a variety of inflammatory reactions in the brain. After stroke, it seems that the innate γδ T cells are the main IL-17 producing cells and that the γδ T cell activation constitutes an early and mainly damaging immune response in stroke. Effector mechanism of γδ T cell derived IL-17 in the ischemic brain include the induction of metalloproteinases, proinflammatory cytokines and neutrophil attracting chemokines, leading to a further amplification of the detrimental inflammatory response. In this review, we will give an overview on the concepts of γδ T cells and IL-17 in stroke pathophysiology and on their potential importance for human disease conditions.
authors.affiliation: Department of Neurology, University Medical Center Hamburg-Eppendorf Hamburg, Germany.
authors.forename: Mathias
authors.initials: M
authors.lastname: Gelderblom
authors.affiliation: Department of Neurology, University Medical Center Hamburg-Eppendorf Hamburg, Germany.
authors.forename: Priyadharshini
authors.initials: P
authors.lastname: Arunachalam
authors.affiliation: Department of Neurology, University Medical Center Hamburg-Eppendorf Hamburg, Germany.
authors.forename: Tim
authors.initials: T
authors.lastname: Magnus
keywords: IL-17; brain; inflammation; ischemia; lymphocyte; neutrophils; stroke; γδ T cell