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591 results on '"Kwekkeboom, Jaap"'

152. Polarized release of hepatic microRNAs into bile and serum in response to cellular injury and impaired liver function

Author

Verhoeven, Cornelia J., primary, Farid, Waqar R. R., additional, Roest, Henk P., additional, Ramakrishnaiah, Vedashree, additional, de Ruiter, Petra E., additional, de Jonge, Jeroen, additional, Kwekkeboom, Jaap, additional, Metselaar, Herold J., additional, Tilanus, Hugo W., additional, Kazemier, Geert, additional, Ijzermans, Jan N. M., additional, and van der Laan, Luc J. W., additional

Published
2015
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153. Cytomegalovirus-Induced Expression of CD244 after Liver Transplantation Is Associated with CD8+ T Cell Hyporesponsiveness to Alloantigen

Author

de Mare-Bredemeijer, Emmy L. D., primary, Shi, Xiao-lei, additional, Mancham, Shanta, additional, van Gent, Rogier, additional, van der Heide-Mulder, Marieke, additional, de Boer, Renate, additional, Heemskerk, Mirjam H. M., additional, de Jonge, Jeroen, additional, van der Laan, Luc J. W., additional, Metselaar, Herold J., additional, and Kwekkeboom, Jaap, additional

Published
2015
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154. Human Graft-Derived Mesenchymal Stromal Cells Potently Suppress Alloreactive T-Cell Responses

Author

de Mare-Bredemeijer, Emmy L.D., primary, Mancham, Shanta, additional, Verstegen, Monique M.A., additional, de Ruiter, Petra E., additional, van Gent, Rogier, additional, O'Neill, David, additional, Tilanus, Hugo W., additional, Metselaar, Herold J., additional, de Jonge, Jeroen, additional, Kwekkeboom, Jaap, additional, Hall, Sean R.R., additional, and van der Laan, Luc J.W., additional

Published
2015
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155. GITR engagement in combination with CTLA-4 blockade completely abrogates immunosuppression mediated by human liver tumor-derived regulatory T cellsex vivo

Author

Pedroza-Gonzalez, Alexander, primary, Zhou, Guoying, additional, Singh, Simar Pal, additional, Boor, Patrick PC, additional, Pan, Qiuwei, additional, Grunhagen, Dirk, additional, de Jonge, Jeroen, additional, Tran, TC Khe, additional, Verhoef, Cornelis, additional, IJzermans, Jan NM, additional, Janssen, Harry LA, additional, Biermann, Katharina, additional, Kwekkeboom, Jaap, additional, and Sprengers, Dave, additional

Published
2015
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157. Tumor-infiltrating plasmacytoid dendritic cells promote immunosuppression by Tr1 cells in human liver tumors

Author

Pedroza-Gonzalez, Alexander, primary, Zhou, Guoying, additional, Vargas-Mendez, Ernesto, additional, Boor, Patrick PC, additional, Mancham, Shanta, additional, Verhoef, Cornelis, additional, Polak, Wojciech G, additional, Grünhagen, Dirk, additional, Pan, Qiuwei, additional, Janssen, Harry LA, additional, Garcia-Romo, Gina S, additional, Biermann, Katharina, additional, Tjwa, Eric TTL, additional, IJzermans, Jan NM, additional, Kwekkeboom, Jaap, additional, and Sprengers, Dave, additional

Published
2015
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158. Increased Incidence of Early De Novo Cancer in Liver Graft Recipients Treated with Cyclosporine: An Association with C-2 Monitoring and Recipient Age

Author

Tjon, Angela, Sint Nicolaas, Jerome, Kwekkeboom, Jaap, de Man, Rob, Kazemier, G, Tilanus, Hugo, Hansen, Bettina, van der Laan, Luc, Tha-In, Thanyalak, Metselaar, Herold, Gastroenterology & Hepatology, and Surgery

Subjects
SDG 3 - Good Health and Well-being
Abstract

The goal of this study was to determine the risk factors for de novo cancer after liver transplantation (LTx). Retrospective analyses were performed in 385 LTx patients who underwent transplantation between 1986 and 2007. In total, 50 (13.0%) recipients developed de novo malignancy. The cumulative incidence of de novo cancer at 1, 5, 10, and 15 years after LTx was 2.9% +/- 0.9%, 10.5%+- 1.8%, 19.4% +/- 3.0%, and 33.6% +/- 6.8%, respectively. The standardized incidence ratio of malignancy in LTx patients compared to the general population was 2.2 (95% confidence interval: 1.6-2.8). After excluding posttransplant lymphoproliferative disorder and skin cancer, patients with de novo cancer had a significantly lower survival rate compared to recipients who remained cancer-free. The identified univariate risk factors for de novo cancer were cyclosporine A (CsA) treatment, time period of LTx, and recipient age. In multivariate analysis, only CsA treatment emerged as an independent risk factor for de novo cancer, which was attributed to more aggressive cancer types. A surprising finding was that CsA treatment specifically enhanced cancer risk in patients who underwent transplantation after 2004, when C-2 monitoring (blood concentration at 2 hours postdose) was introduced. In addition, these patients showed a significantly lower acute rejection rate, which might reflect a more robust immunosuppressive status caused by the CsA-C-2 regimen. When age was considered, only patients

Published
2010

159. Calcineurin Inhibitor Tacrolimus Does Not Interfere with the Suppression of Hepatitis C Virus Infection by Interferon-alpha

Author

Pan, Qiuwei, Metselaar, Herold, Ruiter, Petra, Kwekkeboom, Jaap, Tilanus, Hugo, Janssen, HLA, van der Laan, Luc, Gastroenterology & Hepatology, and Surgery

Subjects
SDG 3 - Good Health and Well-being
Abstract

Immunosuppression considerably affects hepatitis C virus (HCV) recurrence and the outcome of antiviral treatment after liver transplantation. Recent findings have suggested that the calcineurin inhibitor tacrolimus (Tac), unlike cyclosporine A (CsA), interferes with the antiviral activity of interferon-alpha (IFN-alpha) in vitro. The aim of this study was to more extensively investigate the effects of calcineurin inhibitors on IFN-alpha signaling and antiviral activity in subgenomic and infectious HCV models. Treatment with Tac and CsA did not affect Huh7 cell proliferation at doses of 10 to 500 ng/mL; however, it completely inhibited T cell proliferation. In contrast to previous reports, Tac had no effect on IFN-alpha-stimulated reporter gene expression, even at the dose of 5 mu g/mL. Furthermore, in Huh7 subgenomic HCV replicon cells, treatment with Tac had no significant effect on the suppression of viral replication by IFN-alpha. In the infectious HCV model, treatment with IFN-alpha effectively inhibited both viral RNA replication and de novo production of virus particles, and neither was attenuated at any concentration of Tac. CsA had no significant effect on IFN-alpha-stimulated reporter gene expression; however, as shown previously, a combination of CsA (at 500 ng/mL and higher) and IFN-a resulted in enhanced inhibition of viral replication in both the subgenomic and infectious HCV models. In conclusion, our study shows no evidence that Tac or CsA interferes with IFN-alpha-mediated inhibition of HCV replication and virion production in vitro. Therefore, no further mechanistic arguments have been found to break the clinical controversy about the choice of calcineurin inhibitors during posttransplantation antiviral therapy. Liver Transpl 16:520-526, 2010. (C) 2010 AASLD.

Published
2010

162. Unphosphorylated ISGF3 drives constitutive expression of interferon-stimulated genes to protect against viral infections.

Author

Wenshi Wang, Yuebang Yin, Lei Xu, Junhong Su, Fen Huang, Yijin Wang, Boor, Patrick P. C., Kan Chen, Wenhui Wang, Wanlu Cao, Xinying Zhou, Pengyu Liu, van der Laan, Luc J. W., Kwekkeboom, Jaap, Peppelenbosch, Maikel P., and Qiuwei Pan

Subjects
INTERFERONS, TRANSCRIPTION factors, PHOSPHORYLATION, CELL lines, VIRUS diseases, GENES
Abstract

Interferon (IFN)-stimulated genes (ISGs) are antiviral effectors that are induced by IFNs through the formation of a tripartite transcription factor ISGF3, which is composed of IRF9 and phosphorylated forms of STAT1 and STAT2. However, we found that IFN-independent ISG expression was detectable in immortalized cell lines, primary intestinal and liver organoids, and liver tissues. The constitutive expression of ISGs was mediated by the unphosphorylated ISGF3 (U-ISGF3) complex, consisting of IRF9 together with unphosphorylated STAT1 and STAT2. Under homeostatic conditions, STAT1, STAT2, and IRF9 were found in the nucleus. Analysis of a chromatin immunoprecipitation sequencing data set revealed that STAT1 specifically bound to the promoters of ISGs even in the absence of IFNs. Knockdown of STAT1, STAT2, or IRF9 by RNA interference led to the decreased expression of various ISGs in Huh7.5 human liver cells, which was confirmed in mouse embryonic fibroblasts (MEFs) from STAT1-/-, STAT2-/-, or IRF9-/- mice. Furthermore, decreased ISG expression was accompanied by increased replication of hepatitis C virus and hepatitis E virus. Conversely, simultaneous overexpression of all ISGF3 components, but not any single factor, induced the expression of ISGs and inhibited viral replication; however, no phosphorylated STAT1 and STAT2 were detected. A phosphorylation-deficient STAT1 mutant was comparable to the wild-type protein in mediating the IFN-independent expression of ISGs and antiviral activity, suggesting that ISGF3 works in a phosphorylationindependent manner. These data suggest that the U-ISGF3 complex is both necessary and sufficient for constitutive ISG expression and antiviral immunity under homeostatic conditions. [ABSTRACT FROM AUTHOR]

Published
2017
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164. Kupffer Cells Interact With Hepatitis B Surface Antigen In Vivo and In Vitro, Leading to Proinflammatory Cytokine Production and Natural Killer Cell Function

Author

Boltjes, Arjan, primary, van Montfoort, Nadine, additional, Biesta, Paula J., additional, Op den Brouw, Marjoleine L., additional, Kwekkeboom, Jaap, additional, van der Laan, Luc J.W., additional, Janssen, Harry L.A., additional, Boonstra, André, additional, and Woltman, Andrea M., additional

Published
2014
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165. Rotterdam: Main port for organ transplantation research in the Netherlands

Author

Kwekkeboom, Jaap, primary, van der Laan, Luc J.W., additional, Betjes, Michiel G.H., additional, Manintveld, Olivier C., additional, Hoek, Rogier A.S., additional, Cransberg, Karlien, additional, de Bruin, Ron W.F., additional, Dor, Frank J.M.F., additional, de Jonge, Jeroen, additional, Boor, Patrick P.C., additional, van Gent, Rogier, additional, van Besouw, Nicole M., additional, Boer, Karin, additional, Litjens, Nicolle H.R., additional, Hesselink, Dennis A., additional, Hoogduijn, Martin J., additional, Massey, Emma, additional, Rowshani, Ajda T., additional, van de Wetering, Jacqueline, additional, de Jong, Huib, additional, Hendriks, Rudi W., additional, Metselaar, Herold J., additional, van Gelder, Teun, additional, Weimar, Willem, additional, IJzermans, Jan N.M., additional, and Baan, Carla C., additional

Published
2014
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166. Genetic variance in ABCB1 and CYP3A5 does not contribute toward the development of chronic kidney disease after liver transplantation

Author

Tapirdamaz, Özlem, primary, Hesselink, Dennis A., additional, el Bouazzaoui, Samira, additional, Azimpour, Mohammad, additional, Hansen, Bettina, additional, van der Laan, Luc J.W., additional, Polak, Wojciech G., additional, Kwekkeboom, Jaap, additional, van Schaik, Ron H.N., additional, van Gelder, Teun, additional, and Metselaar, Herold J., additional

Published
2014
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168. Identifying genetic risk variants for coronary heart disease in familial hypercholesterolemia: an extreme genetics approach

Author

Versmissen, Jorie, primary, Oosterveer, Daniëlla M, additional, Yazdanpanah, Mojgan, additional, Dehghan, Abbas, additional, Hólm, Hilma, additional, Erdman, Jeanette, additional, Aulchenko, Yurii S, additional, Thorleifsson, Gudmar, additional, Schunkert, Heribert, additional, Huijgen, Roeland, additional, Vongpromek, Ranitha, additional, Uitterlinden, André G, additional, Defesche, Joep C, additional, van Duijn, Cornelia M, additional, Mulder, Monique, additional, Dadd, Tony, additional, Karlsson, Hróbjartur D, additional, Ordovas, Jose, additional, Kindt, Iris, additional, Jarman, Amelia, additional, Hofman, Albert, additional, van Vark-van der Zee, Leonie, additional, Blommesteijn-Touw, Adriana C, additional, Kwekkeboom, Jaap, additional, Liem, Anho H, additional, van der Ouderaa, Frans J, additional, Calandra, Sebastiano, additional, Bertolini, Stefano, additional, Averna, Maurizio, additional, Langslet, Gisle, additional, Ose, Leiv, additional, Ros, Emilio, additional, Almagro, Fátima, additional, de Leeuw, Peter W, additional, Civeira, Fernando, additional, Masana, Luis, additional, Pintó, Xavier, additional, Simoons, Maarten L, additional, Schinkel, Arend FL, additional, Green, Martin R, additional, Zwinderman, Aeilko H, additional, Johnson, Keith J, additional, Schaefer, Arne, additional, Neil, Andrew, additional, Witteman, Jacqueline CM, additional, Humphries, Steve E, additional, Kastelein, John JP, additional, and Sijbrands, Eric JG, additional

Published
2014
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170. Genetic variation in TNFA predicts protection from severe bacterial infections in patients with end-stage liver disease awaiting liver transplantation

Author

Senkerikova, Renata, primary, de Mare-Bredemeijer, Emmeloes, additional, Frankova, Sona, additional, Roelen, Dave, additional, Visseren, Thijmen, additional, Trunecka, Pavel, additional, Spicak, Julius, additional, Metselaar, Herold, additional, Jirsa, Milan, additional, Kwekkeboom, Jaap, additional, and Sperl, Jan, additional

Published
2014
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172. T-cell suppression mediated by regulatory T cells infiltrating hepatic tumors can be overcome by GITRL treatment

Author

Pedroza Gonzalez, Alexander, Kwekkeboom, Jaap, Sprengers, Dave, Pedroza Gonzalez, Alexander, Kwekkeboom, Jaap, and Sprengers, Dave

Abstract

Recently, we reported the accumulation of CD4+ FOXP3+ regulatory T cells (Tregs) within the tumor mass of patients bearing liver cancer. Tumor-infiltrating Tregs (TiTreg) are active and potent suppressors of antitumor immunity. Importantly, treatment with GITR L reduced the immunosuppression mediated by TiTreg.

Published
2013

174. MicroRNA profiles in graft preservation solution are predictive of ischemic-type biliary lesions after liver transplantation

Author

Verhoeven, Cornelia J., primary, Farid, Waqar R.R., additional, de Ruiter, Petra E., additional, Hansen, Bettina E., additional, Roest, Henk P., additional, de Jonge, Jeroen, additional, Kwekkeboom, Jaap, additional, Metselaar, Herold J., additional, Tilanus, Hugo W., additional, Kazemier, Geert, additional, and van der Laan, Luc J.W., additional

Published
2013
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177. Defining Early Human NK Cell Developmental Stages in Primary and Secondary Lymphoid Tissues

Author

Eissens, DN, Spanholtz, J, van der Meer, A, van Cranenbroek, B, Dolstra, H, Kwekkeboom, Jaap, Preijers, FWMB, Joosten, I, Eissens, DN, Spanholtz, J, van der Meer, A, van Cranenbroek, B, Dolstra, H, Kwekkeboom, Jaap, Preijers, FWMB, and Joosten, I

Abstract

A better understanding of human NK cell development in vivo is crucial to exploit NK cells for immunotherapy. Here, we identified seven distinctive NK cell developmental stages in bone marrow of single donors using 10-color flow cytometry and found that NK cell development is accompanied by early expression of stimulatory co-receptor CD244 in vivo. Further analysis of cord blood (CB), peripheral blood (PB), inguinal lymph node (inLN), liver lymph node (liLN) and spleen (SPL) samples showed diverse distributions of the NK cell developmental stages. In addition, distinctive expression profiles of early development marker CD33 and C-type lectin receptor NKG2A between the tissues, suggest that differential NK cell differentiation may take place at different anatomical locations. Differential expression of NKG2A and stimulatory receptors (e.g. NCR, NKG2D) within the different subsets of committed NK cells demonstrated the heterogeneity of the CD56(bright)CD16(+/-) and CD56(dim)CD16(+) subsets within the different compartments and suggests that microenvironment may play a role in differential in situ development of the NK cell receptor repertoire of committed NK cells. Overall, differential in situ NK cell development and trafficking towards multiple tissues may give rise to a broad spectrum of mature NK cell subsets found within the human body.

Published
2012

178. Detailed Kinetics of the Direct Allo-Response in Human Liver Transplant Recipients: New Insights from an Optimized Assay

Author

Tapirdamaz, Ozlem, Mancham, Shanta, van der Laan, Luc, Kazemier, G, Thielemans, K, Metselaar, Herold, Kwekkeboom, Jaap, Tapirdamaz, Ozlem, Mancham, Shanta, van der Laan, Luc, Kazemier, G, Thielemans, K, Metselaar, Herold, and Kwekkeboom, Jaap

Abstract

Conventional assays for quantification of allo-reactive T-cell precursor frequencies (PF) are relatively insensitive. We present a robust assay for quantification of PF of T-cells with direct donor-specificity, and establish the kinetics of circulating donor-specific T cells after liver transplantation (LTx). B cells from donor splenocytes were differentiated into professional antigen-presenting cells by CD40-engagement (CD40-B cells). CFSE-labelled PBMC from LTx-recipients obtained before and at several time points after LTx, were stimulated with donor-derived or 3(rd) party CD40-B cells. PF of donor-specific T cells were calculated from CFSE-dilution patterns, and intracellular IFN-gamma was determined after re-stimulation with CD40-B cells. Compared to splenocytes, stimulations with CD40-B cells resulted in 3 to 5-fold higher responding T-cell PF. Memory and naive T-cell subsets responded equally to allogeneic CD40-B cell stimulation. Donor-specific CD4(+) and CD8(+) T-cell PF ranged from 0.5 to 19% (median: 5.2%). One week after LTx, PF of circulating donor-specific CD4(+) and CD8(+) T cells increased significantly, while only a minor increase in numbers of T cells reacting to 3(rd) party allo-antigens was observed. One year after LTx numbers of CD4(+) and CD8(+) T cells reacting to donor antigens, as well as those reacting to 3(rd) party allo-antigens, were slightly lower compared to pre-transplant values. Moreover, CD4(+) and CD8(+) T cells responding to donor-derived, as well as those reacting to 3(rd) party CD40-B cells, produced less IFN-gamma. In conclusion, our alternative approach enables detection of allo-reactive human T cells at high frequencies, and after application we conclude that donor-specific T-cell PF increase immediately after LTx. However, no evidence for a specific loss of circulating T-cells recognizing donor allo-antigens via the direct pathway up to 1 year after LTx was obtained, underscoring the relative insensitiveness of previous assa

Published
2010

181. Polarized release of hepatic micro RNAs into bile and serum in response to cellular injury and impaired liver function.

Author

Verhoeven, Cornelia J., Farid, Waqar R. R., Roest, Henk P., Ramakrishnaiah, Vedashree, Ruiter, Petra E., Jonge, Jeroen, Kwekkeboom, Jaap, Metselaar, Herold J., Tilanus, Hugo W., Kazemier, Geert, Ijzermans, Jan N. M., and Laan, Luc J. W.

Subjects
RNA, SERUM, LIVER cells, LIVER transplantation, PROTEINS
Abstract

Background & Aims Extracellular micro RNAs (mi RNAs) in serum and bile are currently under intense investigation for biomarker purposes in liver disease. However, the directions and pathways by which mi RNAs are released from hepatic cells remains largely unknown. Here, we investigated the release of hepatocyte and cholangiocyte-derived mi RNAs ( HDmiRs and CDmiRs) into blood and bile during various (patho)physiological hepatic conditions. Methods Mi RNA release was analysed using longitudinally collected tissue and paired bile and serum samples ( n = 124) that were obtained from liver transplant recipients during follow-up. Results Cell-type specificity of HDmiRs and CDmiRs was confirmed in liver and common bile duct biopsies ( P < 0.001). Analysis of paired bile and serum samples showed up to 20-times higher mi RNA-levels in bile compared to serum ( P < 0.0001). Fractionation of bile showed the majority of mi RNAs being present in the unpelletable supernatant, where protein conjunctions protect mi RNAs against degradation ( P < 0.0001). During episodes of liver injury and histologically proven rejection in liver transplant recipients, relative HDmiR-levels in bile decreased while its levels in serum increased ( P ≤ 0.015). Simultaneously, relative CDmiR-levels in bile significantly increased, while their levels in serum decreased. Related to liver excretory function, a strong positive correlation was observed between HDmiR-122 levels and bilirubin excretion into bile ( R = 0.694, P < 0.0001), whereas CDmiRs showed an inverse correlation ( P < 0.05). Conclusion During impaired excretory function and injury, the liver shows polarized release of extracellular HDmiRs and CDmiRs. This sheds new light on the biology of hepatic mi RNA release which is relevant for the interpretation of hepatic mi RNAs as biomarkers. [ABSTRACT FROM AUTHOR]

Published
2016
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185. Secreted Factors of Human Liver-Derived Mesenchymal Stem Cells Promote Liver Regeneration Early After Partial Hepatectomy

Author

Fouraschen, Suomi M.G., primary, Pan, Qiuwei, additional, de Ruiter, Petra E., additional, Farid, Waqar R.R., additional, Kazemier, Geert, additional, Kwekkeboom, Jaap, additional, Ijzermans, Jan N.M., additional, Metselaar, Herold J., additional, Tilanus, Hugo W., additional, de Jonge, Jeroen, additional, and van der Laan, Luc J.W., additional

Published
2012
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193. Migration of allosensitizing donor myeloid dendritic cells into recipients after liver transplantation

Author

Bosma, Brenda M., primary, Metselaar, Herold J., additional, Gerrits, Jeroen H., additional, van Besouw, Nicole M., additional, Mancham, Shanta, additional, Groothuismink, Zwier M. A., additional, Boor, Patrick P. C., additional, van der Laan, Luc J. W., additional, Tilanus, Hugo W., additional, Kuipers, Ernst J., additional, and Kwekkeboom, Jaap, additional

Published
2009
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194. Conversion From Calcineurin Inhibitor to Mycophenolate Mofetil-Based Immunosuppression Changes the Frequency and Phenotype of CD4+FOXP3+ Regulatory T Cells

Author

Demirkiran, Ahmet, primary, Sewgobind, Varsha D. K. D., additional, van der Weijde, Joyce, additional, Kok, Alice, additional, Baan, Carla C., additional, Kwekkeboom, Jaap, additional, Tilanus, Hugo W., additional, Metselaar, Herold J., additional, and van der Laan, Luc J. W., additional

Published
2009
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