CMV-induced class II antigen expression in various rat organs

Ustinov, Jarkko; Loginov, Raisa; Bruggeman, Cathrien A.; Suni, Jukka; Häyry, P; Lautenschlager, Irmeli

doi:10.1007/bf00327161

Cited by 9 publications

(7 citation statements)

References 26 publications

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“…However, it is consistent with previous studies indicating that rat endothelium does not express MHC class II constitutively,20 but expression can be induced in retina, brain, liver, kidney21,22 and on heart allotransplants23 by immune upregulation.…”

Section: Discussionsupporting

confidence: 93%

In vivo observations of cell trafficking in allotransplanted vascularized skin flaps and conventional skin grafts

Horner

Ferguson

Randolph

et al. 2010

Journal of Plastic, Reconstructive & Aesthetic Surgery

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SummaryThe problem of allogeneic skin rejection is a major limitation to more widespread application of clinical composite tissue allotransplantation (CTA). Previous research examining skin rejection has mainly studied rejection of conventional skin grafts (CSG) using standard histological techniques. The aim of this study was to objectively assess if there were differences in the immune response to CSG and primarily vascularized skin in composite tissue allotransplants (SCTT) using in vivo techniques in order to gain new insights in to the immune response to skin allotransplants.CSG and SCTT were transplanted from standard Lewis (LEW) ad Wistar Furth (WF) to recipient transgenic green fluorescent Lewis rats (LEW-GFP). In vivo confocal microscopy was used to observe cell trafficking within skin of the transplants. In addition, immunohistochemical staining was performed on skin biopsies to reveal possible expression of class II major histocompatibility antigens.A difference was observed in the immune response to SCTT compared to CSG. SCTT had a greater density cellular infiltrate than CSG (p < 0.03) that was focused more at the center of the transplant (p < 0.05) than at the edges, likely due to the immediate vascularization of the skin. Recipient dendritic cells were only observed in rejecting SCTT, not CSG. Furthermore, dermal endothelial class II MHC expression was only observed in allogeneic SCTT. The immune response in both SCTT and CSG was focused on targets in the dermis, with infiltrating cells clustering around hair follicles (CSG and SCTT; p < 0.01) and blood vessels (SCTT; p < 0.01) in allogeneic transplants. This study suggests that there are significant differences between rejection of SCTT and CSG that may limit the relevance of much of the historical data on skin graft rejection when applied to composite tissue allotransplantation. Furthermore, the use of novel in vivo techniques identified

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Section: Discussionsupporting

confidence: 93%

In vivo observations of cell trafficking in allotransplanted vascularized skin flaps and conventional skin grafts

Horner

Ferguson

Randolph

et al. 2010

Journal of Plastic, Reconstructive & Aesthetic Surgery

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“…Recent studies have also demonstrated persistence of CMV DNA in bile duct epithelium and endothelial cells of grafts with chronic rejection (19). CMV may have a direct effect on infected cells and an indirect immune effect associated with enhanced expression of HLA antigens and adhesion molecules on biliary and endothelial cells (20). This might explain why CMV precedes LAR as shown in our study.…”

Section: Discussionmentioning

confidence: 99%

Late acute rejection after liver transplantation impacts patient survival

Uemura¹,

Ikegami²,

Sanchez³

et al. 2008

Clinical Transplantation

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Hepatic allograft rejection still remains an important problem following liver transplantation. Early acute rejection, occurring within three months of transplant, is a common event and usually of lesser significance with respect to prognosis than other non-immune-related post-transplant morbidities. However, little is known about late acute rejection (LAR) including factors affecting its occurrence and long-term outcome. In this study, we analyzed LAR including the incidence, clinical risk factors, patient survival, and graft survival. LAR was defined as acute cellular rejection later than six months after liver transplant. Adult patients who had a minimum of 24 months of graft survival were included in this study. A total of 1604 case records of consecutive adult patients (over age 18 yr) who underwent liver transplant between 1985 and 2003 were reviewed. Of the 1604 patients, 305 (19.0%) developed LAR. Patients with primary diagnoses of autoimmune hepatitis, primary biliary cirrhosis, and primary sclerosing cholangitis had higher incidences of LAR, while patients with metabolic disease and retransplant had lower incidence of LAR (p = 0.0024). The LAR group had more female and younger recipients than the no LAR group (p = 0.0026, p = 0.0131, respectively). Patient survival as well as graft survival were significantly lower in the LAR group (p = 0.0083, p = 0.0075, respectively). PTLD was the only significant independent predictor of late rejection. The careful management and treatment of PTLD, especially immunosuppressive management, is important to prevent LAR, which is related to poorer patient survival.

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“…The finding that R33 is essential for virus replication in salivary glands is also supported by the inability to detect class II MHC expression in the salivary gland epithelium of RCMV⌬R33-infected rats. Class II MHC expression is evoked by RCMV infection of rat heart endothelium (50), liver and kidney cells (51), and salivary gland epithelium (Fig. 10).…”

Section: Discussionmentioning

confidence: 99%

The R33 G Protein-Coupled Receptor Gene of Rat Cytomegalovirus Plays an Essential Role in the Pathogenesis of Viral Infection

Beisser

Vink

Dam

et al. 1998

J Virol

134

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We have identified a rat cytomegalovirus (RCMV) gene that encodes a G-protein-coupled receptor (GCR) homolog. This gene (R33) belongs to a family that includes the human cytomegalovirus UL33 gene. R33 was found to be transcribed during the late phase of RCMV infection in rat embryo fibroblasts. Unlike the mRNAs from all the other members of the UL33 family that have been studied to date, the R33 mRNA is not spliced. To study the function of the R33 gene, we constructed an RCMV strain in which the R33 open reading frame is disrupted. The mutant strain (RCMVΔR33) did not show differences in replication from wild-type RCMV upon infection of several rat cell types in vitro. However, marked differences were seen between the mutant and wild-type strain in the pathogenesis of infection in immunocompromised rats. First, the mutant strain induced a significantly lower mortality than the wild-type virus did. Second, in contrast to wild-type RCMV, the mutant strain did not efficiently replicate in the salivary gland epithelial cells of immunocompromised rats. Although viral DNA was detected in salivary glands of RCMVΔR33-infected rats up to 14 days postinfection, it could not be detected at later time points. This indicates that although the strain with R33 deleted is probably transported to the salivary glands in a similar fashion to that for wild-type virus, the mutant virus is not able to either enter or replicate in salivary gland epithelial cells. We conclude that the RCMV R33 gene plays a vital role in the pathogenesis of infection.

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CMV-induced class II antigen expression in various rat organs

Cited by 9 publications

References 26 publications

In vivo observations of cell trafficking in allotransplanted vascularized skin flaps and conventional skin grafts

In vivo observations of cell trafficking in allotransplanted vascularized skin flaps and conventional skin grafts

Late acute rejection after liver transplantation impacts patient survival

The R33 G Protein-Coupled Receptor Gene of Rat Cytomegalovirus Plays an Essential Role in the Pathogenesis of Viral Infection

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