PMID- 21446970
OWN - NLM
STAT- MEDLINE
DCOM- 20110816
LR  - 20230124
IS  - 1600-6143 (Electronic)
IS  - 1600-6135 (Linking)
VI  - 11
IP  - 4
DP  - 2011 Apr
TI  - Crosstalk between complement and Toll-like receptor activation in relation to 
      donor brain death and renal ischemia-reperfusion injury.
PG  - 660-9
LID - 10.1111/j.1600-6143.2011.03475.x [doi]
AB  - Two central pathways of innate immunity, complement and Toll-like receptors 
      (TLRs), play an important role in the pathogenesis of renal injury inherent to 
      kidney transplantation. Recent findings indicate close crosstalk between 
      complement and TLR signaling pathways. It is suggested that mitogen activated 
      protein kinases (MAPKs) might be the key molecules linking both the complement 
      and TLR pathways together. Complement and TLRs are important mediators of renal 
      ischemia-reperfusion injury (IRI). Besides IRI, complement C3 can also be 
      upregulated and activated in the kidney before transplantation as a direct result 
      of brain death (BD) in the donor. This local upregulation and activation of 
      complement in the donor kidney has been proven to be detrimental for renal 
      allograft outcome. Also TLR4 and several of its major ligands are upregulated by 
      donor BD compared to living donors. Important and in line with the observations 
      above, kidney transplant recipients have a benefit when receiving a kidney from a 
      TLR4 Asp299Gly/Thr399Ile genotypic donor. The role of complement and TLRs and 
      crosstalk between these two innate immune systems in relation to renal injury 
      during donor BD and ischemia-reperfusion are focus of this review. Future 
      strategies to target complement and TLR activation in kidney transplantation are 
      considered.
CI  - (c)2011 The Authors Journal compilation(c)2011 The American Society of 
      Transplantation and the American Society of Transplant Surgeons.
FAU - Damman, Jeffrey
AU  - Damman J
AD  - Surgery Nephrology, University Medical Center Groningen, Groningen, The 
      Netherlands Department of Nephrology, Leiden University Medical Center, Leiden, 
      The Netherlands. j.damman@chir.umcg.nl
FAU - Daha, Mohamed R
AU  - Daha MR
FAU - van Son, Willem J
AU  - van Son WJ
FAU - Leuvenink, Henri G
AU  - Leuvenink HG
FAU - Ploeg, Rutger J
AU  - Ploeg RJ
FAU - Seelen, Marc A
AU  - Seelen MA
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Am J Transplant
JT  - American journal of transplantation : official journal of the American Society of 
      Transplantation and the American Society of Transplant Surgeons
JID - 100968638
RN  - 0 (Toll-Like Receptors)
RN  - 9007-36-7 (Complement System Proteins)
SB  - IM
MH  - Animals
MH  - Brain Death/*physiopathology
MH  - Complement System Proteins/*metabolism
MH  - Humans
MH  - Immunity, Innate
MH  - Kidney Transplantation/*adverse effects
MH  - Reperfusion Injury/*etiology
MH  - Toll-Like Receptors/*metabolism
EDAT- 2011/03/31 06:00
MHDA- 2011/08/17 06:00
CRDT- 2011/03/31 06:00
PHST- 2011/03/31 06:00 [entrez]
PHST- 2011/03/31 06:00 [pubmed]
PHST- 2011/08/17 06:00 [medline]
AID - S1600-6135(22)27883-6 [pii]
AID - 10.1111/j.1600-6143.2011.03475.x [doi]
PST - ppublish
SO  - Am J Transplant. 2011 Apr;11(4):660-9. doi: 10.1111/j.1600-6143.2011.03475.x.