TY  - JOUR
AB  - Currently, lung transplantation outcome remains inferior compared to other solid organ transplantations. A major cause for limited survival after lung transplantation is chronic lung allograft dysfunction (CLAD). Numerous animal models have been developed to investigate CLAD in order to discover adequate treatments. The murine orthotopic lung transplant model has been further optimized over the last years. However, different degrees of genetic mismatch between donor and recipient mice have been used, applying a single, minor, moderate and major genetic mismatch. This review aims to reassess the existing murine mismatch models and to provide a comprehensive overview, with a specific focus on their eventual histopathologic presentation. This will be crucial to leverage this model and to tailor it according to specific research needs.
AU  - Coppens, A.*
AU  - Verleden, S.E.*
AU  - Claes, E.*
AU  - Voet, H.*
AU  - Verleden, G.M.*
AU  - Lapperre, T.S.*
AU  - Yildirim, A.Ö.
AU  - Jungraithmayr, W.*
AU  - Yamada, Y.*
AU  - Peeters, D.J.*
AU  - Hendriks, J.M.H.*
C1  - 71427
C2  - 56145
TI  - Murine orthotopic lung transplant models: A comprehensive overview of genetic mismatch degrees and histopathological insights into chronic lung allograft dysfunction.
JO  - Am. J. Transplant.
PY  - 2024
SN  - 1600-6135
ER  - 

TY  - JOUR
AB  - Platelet activation and thrombus formation have been implicated to be detrimental for intraportal pancreatic islet transplants. The platelet-specific collagen receptor glycoprotein VI (GPVI) plays a key role in thrombosis through cellular activation and the subsequent release of secondary mediators. In aggregometry and in a microfluidic dynamic assay system modeling flow in the portal vein, pancreatic islets promoted platelet aggregation and triggered thrombus formation, respectively. While platelet GPVI deficiency did not affect the initiation of these events, it was found to destabilize platelet aggregates and thrombi in this process. Interestingly, while no major difference was detected in early thrombus formation after intraportal islet transplantation, genetic GPVI deficiency or acute anti-GPVI treatment led to an inferior graft survival and function in both syngeneic mouse islet transplantation and xenogeneic human islet transplantation models. These results demonstrate that platelet GPVI signaling is indispensable in stable thrombus formation induced by pancreatic islets. GPVI deficiency resulted in thrombus destabilization and inferior islet engraftment indicating that thrombus formation is necessary for a successful intraportal islet transplantation in which platelets are active modulators.
AU  - Chen, C.
AU  - Rawat, D.*
AU  - Samikannu, B.*
AU  - Bender, M.*
AU  - Preissner, K.T.*
AU  - Linn, T.*
C1  - 60658
C2  - 49567
CY  - 111 River St, Hoboken 07030-5774, Nj Usa
TI  - Platelet glycoprotein VI-dependent thrombus stabilization is essential for the intraportal engraftment of pancreatic islets.
JO  - Am. J. Transplant.
PB  - Wiley
PY  - 2020
SN  - 1600-6135
ER  - 

TY  - JOUR
AB  - Acute cellular rejection occurs frequently during the first few weeks following liver transplantation. During this period, its molecular phenotype is confounded by peri- and postoperative proinflammatory events. To unambiguously define the molecular profile associated with rejection, we collected sequential biological specimens from 55 patients at least 3 years after liver transplantation who developed rejection during trials of intentional immunosuppression withdrawal. We analyzed liver tissue and blood samples obtained before initiation of drug withdrawal and at rejection, alongside blood samples collected during the weaning process. Gene expression profiling was conducted using whole-genome microarrays and real-time polymerase chain reaction. Rejection resulted in distinct blood and liver tissue transcriptional changes in patients who were either positive or negative for hepatitis C virus (HCV). Gene expression changes were mostly independent from pharmacological immunosuppression, and their magnitude correlated with severity of histological damage. Differential expression of a subset of genes overlapped across all conditions. These were used to define a blood predictive model that accurately identified rejection in HCV-negative, but not HCV-positive, patients. Changes were detectable 1-2 mo before rejection was diagnosed. Our results provide insight into the molecular processes underlying acute cellular rejection in liver transplantation and help clarify the potential utility and limitations of transcriptional biomarkers in this setting.
AU  - Bonaccorsi-Riani, E.*
AU  - Pennycuick, A.*
AU  - Londoño, M.C.*
AU  - Lozano, J.J.*
AU  - Benítez, C.*
AU  - Sawitzki, B.*
AU  - Martínez-Picola, M.*
AU  - Bohne, F.
AU  - Martínez-Llordella, M.*
AU  - Miquel, R.*
AU  - Rimola, A.*
AU  - Sánchez-Fueyo, A.*
C1  - 47229
C2  - 39353
CY  - Hoboken
SP  - 484-496
TI  - Molecular characterization of acute cellular rejection occurring during intentional immunosuppression withdrawal in liver transplantation.
JO  - Am. J. Transplant.
VL  - 16
IS  - 2
PB  - Wiley-blackwell
PY  - 2016
SN  - 1600-6135
ER  - 

TY  - JOUR
AU  - Falk, C.S.*
AU  - Daemen, K.*
AU  - Stevanovic-Meyer, M.*
AU  - Lehner, F.*
AU  - Haller, H.*
AU  - Blume, C.*
AU  - Hammerschmidt, W.
AU  - Zeidler, R.
AU  - Neudoerfl, C.*
C1  - 31866
C2  - 35921
CY  - Hoboken
SP  - 36
TI  - Belatacept can inhibit allo-specific T cell responses in a donor-dependent manner but preserves virus-specific memory T cell-responses.
JO  - Am. J. Transplant.
VL  - 14
PB  - Wiley-Blackwell
PY  - 2014
SN  - 1600-6135
ER  -