The interaction between ischemia–reperfusion and immune responses in the kidney

• Published in: Journal of molecular medicine (Berlin, Germany) Vol. 87; no. 9; pp. 859 - 864
• Main Authors: Jang, Hye Ryoun, Ko, Gang Jee, Wasowska, Barbara A., Rabb, Hamid
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer-Verlag 01-09-2009; Springer Nature B.V
• Subjects: Biomedical and Life Sciences; Biomedicine; Human Genetics; Humans; Immune System Phenomena; Immunity; Internal Medicine; Kidney Diseases - immunology; Kidney Diseases - pathology; Molecular Medicine; Reperfusion Injury - immunology; Review; Ischemia–reperfusion injury; Inflammation; Immune response
• ISSN: 0946-2716; 1432-1440
• DOI: 10.1007/s00109-009-0491-y

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.