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27 results on '"Hove, Tessa"'

10. IL-18-Binding Protein Expression by Endothelial Cells and Macrophages Is Up-Regulated During Active Crohn’s Disease

Author

Corbaz, Anne, primary, ten Hove, Tessa, additional, Herren, Suzanne, additional, Graber, Pierre, additional, Schwartsburd, Boris, additional, Belzer, Ilana, additional, Harrison, Jillian, additional, Plitz, Thomas, additional, Kosco-Vilbois, Marie H., additional, Kim, Soo-Hyun, additional, Dinarello, Charles A., additional, Novick, Daniela, additional, van Deventer, Sander, additional, and Chvatchko, Yolande, additional

Published
2002
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13. Development of chronic colitis is dependent on the cytokine MIF

Author

de Jong, Ype P., primary, Abadia-Molina, Ana C., additional, Satoskar, Abhay R., additional, Clarke, Kareem, additional, Rietdijk, Svend T., additional, Faubion, William A., additional, Mizoguchi, Emiko, additional, Metz, Christine N., additional, Sahli, Mazen Al, additional, ten Hove, Tessa, additional, Keates, Andrew C., additional, Lubetsky, Jodi B., additional, Farrell, Richard J., additional, Michetti, Pierre, additional, van Deventer, Sander J., additional, Lolis, Elias, additional, David, John R., additional, Bhan, Atul K., additional, and Terhorst, Cox, additional

Published
2001
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24. Differential Susceptibility of Multidrug Resistance Protein-1 Deficient Mice to DSS and TNBS-Induced Colitis.

Author

Hove, Tessa Ten, Drillenburg, Paul, Wijnholds, Jan, te Velde, Anje A., and van Deventer, Sander J.H.

Subjects
MULTIDRUG resistance, PROTEIN deficiency, COLITIS
Abstract

The molecular mechanisms underlying inflammatory bowel diseases (IBD) are incompletely characterized. MRP-1, normally expressed in the large and small bowel epithelium, serves as a multidrug resistance protein. In this report we explored the role of MRP1 in IBD. Mrp1-deficient mice (mrp1[sup -/-]) were subjected to two different models of IBD. The mrp1[sup -/-] mice and wild-type (WT) mice showed equal induction of TNBS colitis, a hapten-induced T-cell mediated disease. However, in DSS colitis more severe disease was observed in mrp1[sup -/-] mice. In a survival study, mortality of mrp1[sup -/-] mice was higher. In nonlethal DSS colitis, the mean histological colitis score was significantly higher in mrp1[sup -/-]mice and showed particularly severe epithelial damage. Although endogenous LTB[sub 4] levels were significantly increased in mrp1[sup -/-] mice, treatment with a LTB[sub 4] antagonist did not reduce disease. We conclude that MRP-1 has an important role in the intestinal epithelial resistance to exogenous injury, but MRP-1 does not affect T-lymphocyte mediated mucosal damage. [ABSTRACT FROM AUTHOR]

Published
2002

25. LPS induced translocation of NF-κB occurs only in a subpopulation of CD14-positive mononuclear cells.

Author

ten Hove, Tessa, Vervoordeldonk, Margriet J.B.M., Dekkers, Pascale E.P., Reitsma, Pieter H., and van Deventer, Sander J.H.

Abstract

CD14-receptor occupancy is a potent activator of the ubiquitous transcription factor NF-κB. In resting cells, NF-κB exists as a heterodimer in the cytoplasm bound to its inhibitor IκB. Upon stimulation with lipopolysaccharide (LPS), NF-κB translocates to the nucleus. By means of immunohistochemistry, nuclear translocation of the p65 subunit was detected in LPS-stimulated mononuclear cells at the single-cell level. Double-staining experiments showed nuclear translocation of p65 in only a fraction (< 50%) of the LPS-stimulated CD14-positive cells. In vivo, similar results were obtained. In blood from healthy volunteers who were infused with LPS, only a fraction of the CD14-positive cells showed translocation of the p65 subunit. In conclusion, we identified the translocation of NF-κB after LPS stimulation at the single cell level in vitro and in vivo. Surprisingly, only a subpopulation of CD14-positive cells showed translocation. These data indicate that the mere expression of CD14 alone is insufficient for LPS-responsiveness. [ABSTRACT FROM PUBLISHER]

Published
1999
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26. Expression of CD45RB functionally distinguishes intestinal T lymphocytes in inflammatory bowel disease

Author

Hove, Tessa, The, F. Olle, Berkhout, Marloes, Bruggeman, Joost P., Vyth‐Dreese, Florry A., Slors, J. Frederik M., Deventer, Sander J. H., and Velde, Anje A.

Abstract

The importance of CD45RB expression on T cells was already shown in mice where CD45RBhighexpression determines pathogenic potential. In this study, we analyzed the expression of CD45RA, CD45RB, and CD45RO on CD4+T lymphocytes in the intestinal mucosa and in the circulation of patients with inflammatory bowel disease (IBD). In addition, we studied the cytokine profile of these cells. In the circulation, virtually all CD4+CD45RBhighT cells expressed the naive marker CD45RA, and circulating CD4+CD45RBlowcells expressed the memory marker CD45RO in IBD patients and a control patient population. In contrast, the intestinal CD4+CD45RBhighT cells are in normal controls for 90% CD45RO+. However, in IBD, 27.7% [Crohn’s disease (CD)] and 49% [ulcerative colitis (UC)] of the intestinal CD4+CD45RBhighT cells are CD45RA+. This special CD4CD45RA+T cell in IBD can be found in the lamina propria as well as in lymphoid follicles (confocal laser‐scanning microscopy). The CD4+CD45RBhighT lymphocytes produce significantly less interleukin (IL)‐10 and IL‐4 and produce more tumor necrosis factor α than CD45RBlowT lymphocytes in control patients. CD4+CD45RBlowT cells from IBD patients produced less IL‐10 than CD4+CD45RBlowT lymphocytes of controls, and interferon‐γ production by both T lymphocyte subsets was decreased in IBD. These data indicate that CD and UC are characterized by an influx of CD4+CD45RBhighT lymphocytes. These CD4+CD45RBhighT lymphocytes seem to be important in the pathogenesis of IBD, as they produce more proinflammatory cytokines and less anti‐inflammatory cytokines compared with CD4+CD45RBlowT lymphocytes.

Published
2004
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