Innate immune mechanisms in ischemia/reperfusion

David J. Kaczorowski, Allan Tsung, Timothy R. Billiar*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

56 Scopus citations


Ischemia/reperfusion (I/R) injury remains a major problem in solid organ transplantation, as it adversely impacts both short and long term outcomes. It has been well established that the innate immune system plays a significant role in the pathogenesis of I/R injury. In contrast, the proximal molecular signaling events that initiate activation of the innate immune system are less clear. Recent findings have demonstrated that Toll-like receptors (TLR) play a role in I/R injury. Specifically, TLR4 is central to early activation of the innate immune response in the setting of I/R. Furthermore, recent evidence has shown that endogenous molecules, such as high mobility group box-1 (HMGB1) and others that are released from ischemic, damaged, or dying cells and tissues in the setting I/R, can serve as triggers for activation of the innate immune system and exacerbate tissue injury. This evolving body of literature, which has provided insight into the early molecular events that activate the innate system after I/R, is reviewed here.

Original languageEnglish
Pages (from-to)91-98
Number of pages8
JournalFrontiers in Bioscience - Elite
Volume1 E
Issue number1
StatePublished - 6 Jan 2009
Externally publishedYes


  • Cold storage
  • Danger signals
  • Heparan sulfate
  • High mobility group box-1
  • Hyaluronan
  • Ischemia
  • Reperfusion
  • Review
  • Toll-like receptors
  • Transplantation


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