Title |
γδ T cells as early sensors of tissue damage and mediators of secondary neurodegeneration
|
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Published in |
Frontiers in Cellular Neuroscience, November 2014
|
DOI | 10.3389/fncel.2014.00368 |
Pubmed ID | |
Authors |
Mathias Gelderblom, Priyadharshini Arunachalam, Tim Magnus |
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. |
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Geographical breakdown
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Mexico | 1 | 2% |
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Demographic breakdown
Readers by professional status | Count | As % |
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Student > Ph. D. Student | 14 | 23% |
Researcher | 9 | 15% |
Student > Doctoral Student | 8 | 13% |
Student > Master | 6 | 10% |
Student > Postgraduate | 4 | 7% |
Other | 8 | 13% |
Unknown | 11 | 18% |
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Agricultural and Biological Sciences | 4 | 7% |
Other | 2 | 3% |
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