Journal of Molecular Medicine

, Volume 87, Issue 9, pp 859–864

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

Authors

  • Hye Ryoun Jang
    • Nephrology Division, Department of MedicineJohns Hopkins University School of Medicine
  • Gang Jee Ko
    • Nephrology Division, Department of MedicineJohns Hopkins University School of Medicine
  • Barbara A. Wasowska
    • Department of PathologyJohns Hopkins University School of Medicine
    • Nephrology Division, Department of MedicineJohns Hopkins University School of Medicine
Review

DOI: 10.1007/s00109-009-0491-y

Cite this article as:
Jang, H.R., Ko, G.J., Wasowska, B.A. et al. J Mol Med (2009) 87: 859. doi:10.1007/s00109-009-0491-y

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.

Keywords

Ischemia–reperfusion injury Immune response Inflammation

Copyright information

© Springer-Verlag 2009