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.

journal_name

Front Cell Neurosci

authors

Gelderblom M,Arunachalam P,Magnus T

doi

10.3389/fncel.2014.00368

subject

Has Abstract

pub_date

2014-11-05 00:00:00

pages

368

issn

1662-5102

journal_volume

8

pub_type

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