The interaction between ischemia-reperfusion and immune responses in the kidney.
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.
Jang
Hye Ryoun
HR
Nephrology Division, Department of Medicine, Johns Hopkins University School of Medicine, Ross Building, Room 965, 720 Rutland Avenue, Baltimore, MD 21205, USA.
Ko
Gang Jee
GJ
Wasowska
Barbara A
BA
Rabb
Hamid
H
D006801:Humans; D055633:Immune System Phenomena; D007109:Immunity; D007674:Kidney Diseases / Q000276:immunology* / Q000473:pathology; D015427:Reperfusion Injury / Q000276:immunology*