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- W2288637134 abstract "Introduction: Progression of post-stroke tissue damage is partially driven by an inflammatory response involving different subsets of innate and adaptive immune cells. Functionally diverse T-cell subsets have been associated with beneficial and deleterious effects in lesion development. The role of dendritic cells (DCs), which are crucial for T-cell activation, remains undetermined so far. DCs, which express the CC-chemokine CCL17 are key regulators of Treg- and Th17-cell function. The role of DC-dependent immunomodulation as well as the impact of CCL17 in the pathogenesis of cerebral ischemia has not yet been defined. Methods: Transient middle cerebral ischemia was induced by middle cerebral artery occlusion (MCAO, 30 min) in CCL17-deficient (CCL17E/E), heterozygous (CCL17E/+) and wildtype (WT) adult mice. Following MCAO, mice were tested for functional outcome, infarct volume, CCL17 expression and presence of immune cells by immunofluorescence analysis and flow cytometry. Results: Cerebral ischemia led to worsened functional outcome (p<0.001) and increased infarct lesion size (p<0.05) in CCL17-deficient mice. Immunofluorescence analysis of brain tissues revealed expression of CCL17 within the lesion and the ipsilateral hippocampus. CCL17-deficient brains showed enhanced neutrophil immigration, but decreased monocyte recruitment and microglial activation. Conclusion: Altogether, these results suggest a neuroprotective role of CCL17 in the pathogenesis of ischemia/reperfusion damage." @default.
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- W2288637134 date "2015-02-01" @default.
- W2288637134 modified "2023-09-23" @default.
- W2288637134 title "Abstract T P97: CCL17-deficiency Leads to Worsened Functional Outcome and Increased Lesion Size in Experimental Stroke" @default.
- W2288637134 doi "https://doi.org/10.1161/str.46.suppl_1.tp97" @default.
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