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γδ T cells as early sensors of tissue damage and mediators of secondary neurodegeneration

By Mathias eGelderblom, Priyadharshini eArunachalam and Tim eMagnus

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

Topics: Brain, Inflammation, Ischemia, Neutrophils, Stroke, IL-17, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571
Publisher: Frontiers Media S.A.
Year: 2014
DOI identifier: 10.3389/fncel.2014.00368
OAI identifier: oai:doaj.org/article:b1cb72cc2e9d4155bcf57fc7e2f4da60
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