Abstract
Both innate and adaptive immunity contribute to the pathogenesis of ischemia-reperfusion injury (IRI).During acute phase of kidney IRI,kidney endothelial cells promote inflammation after IRI by increasing adhesion molecule expression and vascular permeability,and tubular epithelial cells increase complement C3 binding and Toll-like receptor 2 and Toll-like receptor 4 expression.Early activation of kidney dendritic cells initiates a cascade of events leading to accumulation of neutrophils,macrophage,natural killer cells,CD4 + T cells and B cells in the early phase of renal IRI.Soluble components of the immune system,such as complement activation production,cytokines and chemokines,also are implicated in the injury and repair of post-ischemic kidneys.Foxp3 + regulatory T cells and alternatively activated macrophage participate in attenuating the inflammation and initiating the repair of kidney IRI,while B lymphocytes limit repair of kidney IRI. Key words: Ischemia-repeffusion injury; Acute kidney injury; Infammation
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