Send to

Choose Destination
See comment in PubMed Commons below
Transplant Rev (Orlando). 2012 Apr;26(2):60-72. doi: 10.1016/j.trre.2011.05.001. Epub 2011 Oct 13.

Emerging role of innate immunity in organ transplantation: part I: evolution of innate immunity and oxidative allograft injury.

Author information

  • 1German Academy for Transplantation Medicine, 81545 Munich, Germany.


The innate immune system is an evolutionarily highly conserved first rapid line of host defense against tissue injury and consists of a whole family of mobile and sessile cells such as antigen-presenting cells, innate lymphocytes, neutrophils, and vascular cells-dendritic cells representing the bridge to development of an adaptive immune response. The system depends on molecules collectively known as pattern recognition receptors to survey the extracellular space and the cytoplasm for the presence of exogenous pathogen-associated molecular patterns derived from microorganisms as well as damage-associated molecular patterns derived from endogenous tissue injury. Among various pattern recognition receptors, Toll-like receptors play central roles in sensing tissue damage and activating the innate immune system following any injury including postischemic reperfusion injury. This part I of a review focuses on reactive oxygen species-mediated reperfusion injury in terms of a canonical injury to every solid allograft that metamorphoses it into an acutely inflamed organ. Sources and mechanisms of reactive oxygen species production during postischemic reperfusion injury are reviewed by stressing a role of reactive oxygen species-producing enzyme systems as well as differentiating between reactive oxygen species production in donor-derived vascular cells and recipient-derived neutrophils. Finally, a potential role of hypoxia-sensing enzyme systems in the generation of reactive oxygen species is being discussed as an evolutionary principle and the critical cause of oxidative injury to allografts during reperfusion in the recipient.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center