Recipient Toll-like receptors contribute to chronic graft dysfunction by both MyD88- and TRIF-dependent signaling.

@article{Wang2010RecipientTR,
  title={Recipient Toll-like receptors contribute to chronic graft dysfunction by both MyD88- and TRIF-dependent signaling.},
  author={Shijun Wang and Christoph Schmaderer and {\'E}va {\'I}risz Kiss and Claudia Schmidt and Mahnaz Bonrouhi and Stefan Porubsky and Norbert Gretz and Liliana Schaefer and Carsten J Kirschning and Zoran V. Popovic and Hermann-Josef Gr{\"o}ne},
  journal={Disease models & mechanisms},
  year={2010},
  volume={3 1-2},
  pages={92-103}
}
Toll-like receptors (TLRs) recognize specific molecular patterns derived from microbial components (exogenous ligands) or stressed cells (endogenous ligands). Stimulation of these receptors leads to a pronounced inflammatory response in a variety of acute animal models. Chronic allograft dysfunction (CAD) was regarded as a candidate disease to test whether TLRs influence chronic fibrosing inflammation. Potential endogenous renal TLR ligands, specifically for TLR2 and TLR4, have now been… CONTINUE READING