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13 results on '"Tielemans, Dennis"'

4. Circulating T Cells of Patients with Nijmegen Breakage Syndrome Show Signs of Senescence

Author

Meijers, Ruud, Dzierzanowska-Fangrat, K, Zborowska, M, Solarska, I, Tielemans, Dennis, Turnhout, Bob, Driessen, Gertjan, van der Burg, Mirjam, Dongen, Jacques, Chrzanowska, KH, Langerak, Ton, Meijers, Ruud, Dzierzanowska-Fangrat, K, Zborowska, M, Solarska, I, Tielemans, Dennis, Turnhout, Bob, Driessen, Gertjan, van der Burg, Mirjam, Dongen, Jacques, Chrzanowska, KH, and Langerak, Ton

Published
2017

5. Circulating T Cells of Patients with Nijmegen Breakage Syndrome Show Signs of Senescence

Author

Meijers, Ruud W. J., primary, Dzierzanowska-Fangrat, Katarzyna, additional, Zborowska, Magdalena, additional, Solarska, Iwona, additional, Tielemans, Dennis, additional, van Turnhout, Bob A. C., additional, Driessen, Gertjan, additional, van der Burg, Mirjam, additional, van Dongen, Jacques J. M., additional, Chrzanowska, Krystyna H., additional, and Langerak, Anton W., additional

Published
2016
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6. Flowcytometrische analyse van 'small samples'

Author

Langerak, Ton, Tielemans, Dennis, Missotten, TOAR, Baarsma, GS, Vermeulen, Joyce, van der Spek, Ashley, Martin-Martin, L, Almeida, J, Flores-Montero, J, Cullen, M, Mejstrikova, E, Wind, Henk, van der Velden, Vincent, Orfao, A, Dongen, Jacques, van Dongen, JJM, Dik, WA, Langerak, AW, van der Velden, VHJ, Hooijkaas, H, Immunology, Internal Medicine, and Ophthalmology

Published
2010

7. Lack of common TCRA and TCRB clonotypes in CD8(+)/TCR alpha beta(+) T-cell large granular lymphocyte leukemia: a review on the role of antigenic selection in the immunopathogenesis of CD8(+) T-LGL

Author

Sandberg, Yorick, Kallemeijn, Martine, Dik, Wim, Tielemans, Dennis, Tettero, Ingrid, Mol, Ellen, Szczepanski, Tomek, Pol, Y (Y.), Darzentas, N, Dongen, Jacques, Langerak, Ton, Sandberg, Yorick, Kallemeijn, Martine, Dik, Wim, Tielemans, Dennis, Tettero, Ingrid, Mol, Ellen, Szczepanski, Tomek, Pol, Y (Y.), Darzentas, N, Dongen, Jacques, and Langerak, Ton

Abstract

Clonal CD8(+)/T-cell receptor (TCR)alpha beta(+) T-cell large granular lymphocyte (T-LGL) proliferations constitute the most common subtype of T-LGL leukemia. Although the etiology of T-LGL leukemia is largely unknown, it has been hypothesized that chronic antigenic stimulation contributes to the pathogenesis of this disorder. In the present study, we explored the association between expanded TCR-V beta and TCR-V alpha clonotypes in a cohort of 26 CD8(+)/TCR alpha beta(+) T-LGL leukemia patients, in conjunction with the HLA-ABC genotype, to find indications for common antigenic stimuli. In addition, we applied purpose-built sophisticated computational tools for an in-depth evaluation of clustering of TCR beta (TCRB) complementarity determining region 3 (CDR3) amino-acid LGL clonotypes. We observed a lack of clear TCRA and TCRB CDR3 homology in CD8(+)/TCR alpha beta(+) T-LGL, with only low level similarity between small numbers of cases. This is in strong contrast to the homology that is seen in CD4(+)/TCR alpha beta(+) T-LGL and TCR gamma delta(+) T-LGL and thus underlines the idea that the LGL types have different etiopathogenesis. The heterogeneity of clonal CD8(+)/TCR alpha beta(+) T-LGL proliferations might in fact suggest that multiple pathogens or autoantigens are involved.

Published
2014

10. Distinct gene expression profiles of acute myeloid/T-lymphoid leukemia with silenced CEBPA and mutations in NOTCH1

Author

Wouters, Bas J., primary, Jordà, Meritxell Alberich, additional, Keeshan, Karen, additional, Louwers, Irene, additional, Erpelinck-Verschueren, Claudia A. J., additional, Tielemans, Dennis, additional, Langerak, Anton W., additional, He, Yiping, additional, Yashiro-Ohtani, Yumi, additional, Zhang, Pu, additional, Hetherington, Christopher J., additional, Verhaak, Roel G. W., additional, Valk, Peter J. M., additional, Löwenberg, Bob, additional, Tenen, Daniel G., additional, Pear, Warren S., additional, and Delwel, Ruud, additional

Published
2007
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11. Identification of a Subgroup of Biphenotypic Myeloid/T-Cell Acute Leukemias with a CEBPA-Mutant Gene Expression Profile, Frequent CEBPA Promoter Hypermethylation and NOTCH1 Mutations.

Author

Wouters, Bas J., primary, Louwers, Irene, additional, Erpelinck-Verschueren, Claudia A.J., additional, Valk, Peter J.M., additional, Tielemans, Dennis, additional, Langerak, Anton W., additional, Tenen, Daniel G., additional, Pear, Warren S., additional, Lowenberg, Bob, additional, and Delwel, Ruud, additional

Published
2006
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12. Distinct gene expression profiles of acute myeloid/T-lymphoid leukemia with silenced CEBPAand mutations in NOTCH1

Author

Wouters, Bas J., Jordà, Meritxell Alberich, Keeshan, Karen, Louwers, Irene, Erpelinck-Verschueren, Claudia A.J., Tielemans, Dennis, Langerak, Anton W., He, Yiping, Yashiro-Ohtani, Yumi, Zhang, Pu, Hetherington, Christopher J., Verhaak, Roel G.W., Valk, Peter J.M., Löwenberg, Bob, Tenen, Daniel G., Pear, Warren S., and Delwel, Ruud

Abstract

Gene expression profiling of acute myeloid leukemia (AML) allows the discovery of previously unrecognized molecular entities. Here, we identified a specific subgroup of AML, defined by an expression profile resembling that of AMLs with mutations in the myeloid transcription factor CCAAT/enhancer-binding protein alpha (C/EBPα), while lacking such mutations. We found that in these leukemias, the CEBPAgene was silenced, which was associated with frequent promoter hypermethylation. The leukemias phenotypically showed aberrant expression of T-cell genes, of which CD7was most consistent. We identified 2 mechanisms that may contribute to this phenotype. First, absence of Cebpaled to up-regulation of specific T-cell transcripts (ie, Cd7and Lck) in hematopoietic stem cells isolated from conditional Cebpaknockout mice. Second, the enhanced expression of TRIB2, which we identify here as a direct target of the T-cell commitment factor NOTCH1, suggested aberrantly activated Notch signaling. Putatively activating NOTCH1mutations were found in several specimens of the newly identified subgroup, while a large set of control AMLs was mutation negative. A gene expression prediction signature allowed the detection of similar cases of leukemia in independent series of AML.

Published
2007
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13. Natural killer cell receptor expression reflects the role of human cytomegalovirus in the pathogenesis of a subset of CD4+ T-cell large granular lymphocytosis

Author

Sáez-Borderías, Andrea, Romo, Neus, Ruiz-Cabello, Francisco, Cantón, Julia, Tielemans, Dennis, Langerak, Anton W., and López-Botet, Miguel

Subjects
*KILLER cells, *CELL receptors, *CYTOMEGALOVIRUSES, *T cells, *LYMPHOCYTES, *HLA histocompatibility antigens
Abstract

Abstract: A high frequency of CD4+ T-cell large granular lymphocyte (T-LGL) lymphocytosis occurs in human leukocyte antigen (HLA) –DRB1*0701 individuals displaying monoclonal expansions of Vβ13.1+ CD4+ T-cell clones, which specifically respond to human cytomegalovirus (HCMV) antigens. We previously reported the expression of natural killer (NK)–cell associated receptors (NKR) by HCMV-specific cytolytic CD4+ T cells from healthy donors. In the present study a high expression of different NKR (i.e., NKG2D, killer Ig-like receptors (KIR), CD94, ILT2) was observed in CD4+ T cells from both Vβ13.1− and Vβ13.1+ CD4+ T-LGL cases. Remarkably, elevated numbers of CD94/NKG2C+ NK cells, previously shown to expand in association to HCMV infection, were preferentially found in Vβ13.1+ T-LGL, further supporting its role in the pathogenesis of a subset of CD4+ T-LGL. [Copyright &y& Elsevier]

Published
2011
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