Abstract
Kidney ischemia–reperfusion injury (IRI) engages both the innate and adaptive immune responses. Cellular mediators of immunity, such as dendritic cells, neutrophils, macrophages, natural killer T, T, and B cells, contribute to the pathogenesis of renal injury after IRI. Postischemic kidneys express increased levels of adhesion molecules on endothelial cells and toll-like receptors on tubular epithelial cells. Soluble components of the immune system, such as complement activation proteins and cytokines, also participate in injury/repair of postischemic kidneys. Experimental studies on the immune response in kidney IRI have resulted in better understanding of the mechanisms underlying IRI and led to the discovery of novel therapeutic and diagnostic targets.
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Acknowledgments
The authors thank Dr. Maria Teresa Gandolfo for the helpful suggestions with the manuscript. HR is supported by the US National Institutes of Health, US National Kidney Foundation, and Talecris Biotech., Inc. grants. BAW is supported by AHA, ROTRF, and Talecris Biotech., Inc. grants. HRJ is supported by the Korea Research Foundation.
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Jang, H.R., Ko, G.J., Wasowska, B.A. et al. The interaction between ischemia–reperfusion and immune responses in the kidney. J Mol Med 87, 859–864 (2009). https://doi.org/10.1007/s00109-009-0491-y
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DOI: https://doi.org/10.1007/s00109-009-0491-y