[31] These data could not be reproduced by other research groups.[34] We also have to take into account that these values do increase during the first days after transplantation, probably due to a rebound phenomenon that reflects immunological activation due to surgery and organ conservation.[31, 34] In pediatric patients, a rise in plasminogen activator inhibitor 1 was noticed before ACR and was suggested as a candidate biomarker.[35] Validation in a larger cohort has not been reported. A Japanese group developed an enzyme-linked immunoassay (ELISA) for the measurement of serum

human myeloid-related protein complex (MRP8/14). MRP8/14 is expressed in activated human granulocytes and monocytes in the inflammatory phase and is involved in the inflammation-related calcium-dependent activation. In liver transplant recipients, a clear association was observed between serum levels and ACR, however, sensitivity selleck and specificity were not published. Furthermore, there is no information regarding the expression of MRP8/14 during infectious complications.[36] However, in kidney transplant recipients, MRP8/14 was also increased during non-viral infections, but

in combination with procalcitonin a discrimination was possible.[37] It seems obvious that the role of the adaptive immune response is well established in the occurrence of ACR. www.selleckchem.com/products/Temsirolimus.html On the other hand, the role of the innate immunity is less clear. The role of Toll-like receptors (TLR), mediators of innate immunity, was studied in ACR. Patients experiencing ACR had significantly higher levels of TLR4 and a greater capacity to produce the pro-inflammatory

cytokines TNF-α and IL-6 before transplantation, but had a downregulation of the TLR4 pathway if they experienced rejection. In contrast, there was no correlation between TLR2 levels and rejection.[38] Apoptosis is an important mechanism of cell death during ACR and this is mediated via Fas ligand. Increased serum levels of soluble Fas antigen have NADPH-cytochrome-c2 reductase been detected in patients during ACR.[39] Finally, several studies illustrate that blood eosinophilia could be an interesting biomarker for ACR.[40, 41] In one study, a positive predictive value of 82% was found but, more interestingly, a negative predictive value of 86%.[42] However, the response was less clear in patients who received steroids and in HCV-infected patients. Although most of these markers do prove a relationship with ACR, only five could be retained as valuable because these showed a clear relationship with the appearance of ACR, could differentiate from other post-transplant complications and were performed on prospective patient series. The characteristics are summarized in Table 1. Other potential biomarkers were α-glutathione S-transferase (α-GST) and π-glutathione S-transferase (π-GST). GST are a family of multifunctional detoxifying enzymes that are implicated in the conjugation of glutathione with several compounds.