Published online Jun 24, 2016. doi: 10.5500/wjt.v6.i2.336
Peer-review started: October 31, 2015
First decision: November 30, 2015
Revised: March 18, 2016
Accepted: April 21, 2016
Article in press: April 22, 2016
Published online: June 24, 2016
Processing time: 237 Days and 14.9 Hours
AIM: To study the impact of association between cytomegalovirus (CMV) pathogenesis with dendritic cell (DC) maturation and function was evaluated in CMV reactivated liver transplanted patients in comparing with non-reactivated ones, and healthy controls.
METHODS: Monocyte derived dendritic cells (MoDCs) was generated from collected ethylenediaminetetraacetic acid-treated blood samples from patient groups and controls. In these groups, expression rates and mean fluorescent intensity of DC markers were evaluated using flowcytometry technique. Secretion of cytokines including: interleukin (IL)-6, IL-12 and IL-23 were determined using enzyme-linked immunosorbent assay methods. The gene expression of toll-like receptor 2 (TLR2), TLR4 and IL-23 were analyzed using in-house real-time polymerase chain reaction protocols.
RESULTS: Results have been shown significant decreases in: Expression rates of MoDC markers including CD83, CD1a and human leukocyte antigen DR (HLA-DR), the mean fluorescence intensitys for CD1a and HLA-DR, and secretion of IL-12 in CMV reactivated compared with non-reactivated liver transplanted patients. On the other hand, significant increases have been shown in the secretions of IL-6 and IL-23 and gene expression levels of TLR2, TLR4 and IL-23 from MoDCs in CMV reactivated compared with non-reactivated liver transplanted recipients.
CONCLUSION: DC functional defects in CMV reactivated recipients, such as decrease in expression of DC maturation markers, increase in secretion of proinflammatory cytokines, and TLRs can emphasize on the importance of CMV infectivity in development of liver rejection in transplanted patients.
Core tip: Cytomegalovirus (CMV) can interfere with maturation and antigen-presenting function of dendritic cell (DC). This interference with DC function could promote viral spread by paralyzing the adaptive immune system. CMV with DC infection induces inflammatory cytokines and activation of the interferon pathway in transplanted patients. DCs undergo lytic viral cycles, can induce late gene expression of CMV, release of infectious virus, and stimulating of T-cell responses resulted to allograft rejection.