Journal
INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 96, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.intimp.2021.107678
Keywords
Stroke; Ischemic; gamma delta T cell; V gamma 4 T cell; CCL20; IL-17A
Categories
Funding
- NSFC [81373155, 81372082]
- Natural Science Foundation Project of Chongqing [CSTC2015JCYJA10064]
- Chongqing Key Laboratory Funding [CQZDSYS201203]
- Science and Technology Innovation Ability Enhancement Special Project of Army Military Medical University [2019XQY12]
- Army Medical University Funding [SWH2017JCZD06]
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The study found that Vγ4 T cells play a crucial role in ischemic brain tissue damage by providing an early source of IL-17A in stroke. Additionally, CCL20 and IL-1β/IL-23 are deeply involved in amplifying inflammatory responses in the brain tissue.
Background: Through amplifying inflammatory cascades, IL-17A produced by gamma delta T cells potently attracts neutrophils to the site of injury for exacerbating ischemic tissue damage. Our goal was to identify the precise role of gamma delta T cell subsets in ischemic brain tissue damage of stroke. Methods: In a model of experimental stroke, we analyzed the functions of V gamma 1 and V gamma 4 T cells on gamma delta T cell-mediated ischemic brain tissue damage of stroke. Results: We identified that, in stroke, V gamma 4 T cells are essential for gamma delta T cell-mediated ischemic brain tissue damage through providing an early source of IL-17A. Both CCL20 and IL-1 beta/IL-23 are deeply involved in V gamma 4 T cellmediated amplification of inflammatory responses: CCL20 might promote V gamma 4 T cells recruit to infract hemisphere, and IL-1 beta/IL-23 powerfully enhance IL-17A production mediated by the infiltrating V gamma 4 T cells. Moreover, V gamma 4 T cell-derived IL-17A enhances both CCL20 and IL-1 beta, and conversely, CCL20 and IL-1 beta further enhance both recruitment and IL-17A production of IL-17A-positive cells, in a classic positive feedback loop. Conclusion: Our data suggest that in the setting of ischemic stroke, V gamma 4 T cell-derived IL-17A, CCL20 and IL-1 beta/IL-23 in infract hemisphere coordinately to amplify inflammatory cascades and exacerbate ischemic tissue damage.
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