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Study type | Study design | Conclusion | Reference |
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Original article | A blunt, weight-drop approach to model TBI in mice. | It was shown that TBI causes the elevation of IL-33, IL-1β, IL-38, TNF-α, IFN-α, and IL-19 in the hippocampus at 3 h time point, and concomitant EI results in the dose-dependent downregulation of IL-33, IL-1β, IL-38, TNF-α, IFN-α, and IL-19. | [24] |
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Original article | Spinal cord of mice was damaged, and recombinant IL-33 was injected. | Addition of wild-type lung-derived ILC2s into the meningeal space of IL-33r-/- animals partially improves recovery after spinal cord injury. IL-33 released after CNS injury not only initiates a local response but also a meningeal one through actions of ILC2s. | [29] |
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Comment | Comment on “The glia-derived alarmin IL-33 orchestrates the immune response and promotes recovery following CNS injury” by Gadani SP, Walsh, J. T., Smirnov, I., Zheng, J. and Kipnis, J. published in neuron in 2015. | Administration of recombinant IL-33 might be beneficial for treating TBI. | [1] |
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Original article | Transient focal ischemia was induced by intraluminal occlusion of the left middle cerebral artery for 1 h with silicone-coated sutures in mice. | IL-33/ST2 signaling was described as a potential immune regulatory mechanism that enhances the expression of IL-10 in M2 microglia and reduces acute ischemic brain injury after stroke. | [28] |
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Original article | Serum ST2 concentrations in 106 healthy controls and 106 severe TBI patients were measured. | Serum ST2 concentrations are significantly related to inflammation. In TBI, it may be a potential diagnostic marker. | [14] |
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Original article | Samples from human TBI microdialysate, tissue sections from human TBI, and mouse models of CNS injury were used. | IL-33 plays a role in neuroinflammation, and microglia/macrophages are cellular targets for this IL following TBI. | [30] |
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