γδ T cells as early sensors of tissue damage and mediators of secondary neurodegeneration
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γδ T cells as early sensors of tissue damage and mediators of secondary neurodegeneration. / Gelderblom, Mathias; Arunachalam, Priyadharshini; Magnus, Tim.
in: FRONT CELL NEUROSCI, Jahrgang 8, 01.01.2014, S. 368.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - γδ T cells as early sensors of tissue damage and mediators of secondary neurodegeneration
AU - Gelderblom, Mathias
AU - Arunachalam, Priyadharshini
AU - Magnus, Tim
PY - 2014/1/1
Y1 - 2014/1/1
N2 - 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.
AB - 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.
U2 - 10.3389/fncel.2014.00368
DO - 10.3389/fncel.2014.00368
M3 - SCORING: Journal article
C2 - 25414640
VL - 8
SP - 368
JO - FRONT CELL NEUROSCI
JF - FRONT CELL NEUROSCI
SN - 1662-5102
ER -