Journal
JOURNAL OF MOLECULAR MEDICINE-JMM
Volume 87, Issue 9, Pages 859-864Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s00109-009-0491-y
Keywords
Ischemia-reperfusion injury; Immune response; Inflammation
Funding
- US National Institutes of Health
- US National Kidney Foundation
- Talecris Biotech., Inc
- AHA
- ROTRF
- Korea Research Foundation
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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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