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3. Bencmark worshop on Pandalus stocks (WKPRAWN)

Author

Lordan, Colm, Lövgren, Johan, Cardinale, M.(Massimiliano), Casas-Sánchez, J.M. (José Miguel), Wall-Andersen, M.(Michael), Baagoe-Buch, T.(Tanja), Bakanev, S.(Sergey), Baker, K.(Krista), Bergenius-Nord, M.(Mikaela), Börjesson, P.(Patrik), Burmeister, A.(Anndorte), Ritzau-Eigaard, O.(Ole), Griffiths, C.(Chris), Hvingel, C.(Carsten), Masnadi, F.(Francesco), Norén, K.(Katja), Orio, A.(Alessandro), Simpson, M.(Mark), Skanes, K.(Katherine), Søvik, G.(Guldborg), Zimmermann, F.(Fabian), Casas-Sánchez, José Miguel, Lordan, Colm, Lövgren, Johan, Cardinale, M.(Massimiliano), Casas-Sánchez, J.M. (José Miguel), Wall-Andersen, M.(Michael), Baagoe-Buch, T.(Tanja), Bakanev, S.(Sergey), Baker, K.(Krista), Bergenius-Nord, M.(Mikaela), Börjesson, P.(Patrik), Burmeister, A.(Anndorte), Ritzau-Eigaard, O.(Ole), Griffiths, C.(Chris), Hvingel, C.(Carsten), Masnadi, F.(Francesco), Norén, K.(Katja), Orio, A.(Alessandro), Simpson, M.(Mark), Skanes, K.(Katherine), Søvik, G.(Guldborg), Zimmermann, F.(Fabian), and Casas-Sánchez, José Miguel

Published
2022

11. Aberrant splicing of the tumor suppressor CYLD promotes the development of chronic lymphocytic leukemia via sustained NF-kappaB signaling

Author

Hahn, M., Burckert, J.-P., Luttenberger, C. A., Klebow, S., Hess, M., Al-Maarri, M., Vogt, M., Reissig, S., Hallek, M., Wienecke-Baldacchino, Anke, Buch, T., Muller, Claire, Pallasch, C. P., Wunderlich, F. T., Waisman, A., and Hovelmeyer, N.

Subjects
immune system diseases, hemic and lymphatic diseases, Genetics & genetic processes [F10] [Life sciences], Génétique & processus génétiques [F10] [Sciences du vivant]
Abstract

The pathogenesis of chronic lymphocytic leukemia (CLL) has been linked to constitutive NF-kappaB activation but the underlying mechanisms are poorly understood. Here we show that alternative splicing of the negative regulator of NF-kappaB and tumor suppressor gene CYLD regulates the pool of CD5(+) B cells through sustained canonical NF-kappaB signaling. Reinforced canonical NF-kappaB activity leads to the development of B1 cell-associated tumor formation in aging mice by promoting survival and proliferation of CD5(+) B cells, highly reminiscent of human B-CLL. We show that a substantial number of CLL patient samples express sCYLD, strongly implicating a role for it in human B-CLL. We propose that our new CLL-like mouse model represents an appropriate tool for studying ubiquitination-driven canonical NF-kappaB activation in CLL. Thus, inhibition of alternative splicing of this negative regulator is essential for preventing NF-kappaB-driven clonal CD5(+) B-cell expansion and ultimately CLL-like disease.

Published
2017

12. Aberrant splicing of the tumor suppressor CYLD promotes the development of chronic lymphocytic leukemia via sustained NF-kappa B signaling

Author

Hahn, M., Buerckert, J-P, Luttenberger, C. A., Klebow, S., Hess, M., Al-Maarri, M., Vogt, M., Reissig, S., Hallek, M., Wienecke-Baldacchino, A., Buch, T., Muller, C. P., Pallasch, C. P., Wunderlich, F. T., Waisman, A., Hoevelmeyer, N., Hahn, M., Buerckert, J-P, Luttenberger, C. A., Klebow, S., Hess, M., Al-Maarri, M., Vogt, M., Reissig, S., Hallek, M., Wienecke-Baldacchino, A., Buch, T., Muller, C. P., Pallasch, C. P., Wunderlich, F. T., Waisman, A., and Hoevelmeyer, N.

Abstract

The pathogenesis of chronic lymphocytic leukemia (CLL) has been linked to constitutive NF-kappa B activation but the underlying mechanisms are poorly understood. Here we show that alternative splicing of the negative regulator of NF-kappa B and tumor suppressor gene CYLD regulates the pool of CD5(+) B cells through sustained canonical NF-kappa B signaling. Reinforced canonical NF-kappa B activity leads to the development of B1 cell-associated tumor formation in aging mice by promoting survival and proliferation of CD5(+) B cells, highly reminiscent of human B-CLL. We show that a substantial number of CLL patient samples express sCYLD, strongly implicating a role for it in human B-CLL. We propose that our new CLL-like mouse model represents an appropriate tool for studying ubiquitination-driven canonical NF-kappa B activation in CLL. Thus, inhibition of alternative splicing of this negative regulator is essential for preventing NF-kappa B-driven clonal CD5(+) B-cell expansion and ultimately CLL-like disease.

Published
2018

13. Cost and affordability of diets modelled on current eating patterns and on dietary guidelines, for New Zealand total population, Maori and Pacific Households

Author

Mackay, S., Buch, T., Vandevijvere, S., Goodwin, R., Korohina, E., Funaki-Tahifote, M., Lee, Andy, Swinburn, B., Mackay, S., Buch, T., Vandevijvere, S., Goodwin, R., Korohina, E., Funaki-Tahifote, M., Lee, Andy, and Swinburn, B.

Abstract

© 2018 by the authors. Licensee MDPI, Basel, Switzerland. The affordability of diets modelled on the current (less healthy) diet compared to a healthy diet based on Dietary Guidelines was calculated for population groups in New Zealand. Diets using common foods were developed for a household of four for the total population, Maori and Pacific groups. Maori and Pacific nutrition expert panels ensured the diets were appropriate. Each current (less healthy) diet was based on eating patterns identified from national nutrition surveys. Food prices were collected from retail outlets. Only the current diets contained alcohol, takeaways and discretionary foods. The modelled healthy diet was cheaper than the current diet for the total population (3.5% difference) and Pacific households (4.5% difference) and similar in cost for Maori households (0.57% difference). When the diets were equivalent in energy, the healthy diet was more expensive than the current diet for all population groups (by 8.5% to 15.6%). For households on the minimum wage, the diets required 27% to 34% of household income, and if receiving income support, required 41–52% of household income. Expert panels were invaluable in guiding the process for specific populations. Both the modelled healthy and current diets are unaffordable for some households as a considerable portion of income was required to purchase either diet. Policies are required to improve food security by lowering the cost of healthy food or improving household income.

Published
2018

14. Roquin recognizes a non-canonical hexaloop structure in the 3'-UTR of Ox40

Author

Janowski, R., Heinz, G.A., Schlundt, A., Wommelsdorf, N., Brenner, S., Gruber, A.R., Blank, M., Buch, T., Buhmann, R., Zavolan, M., Niessing, D., Heissmeyer, V., and Sattler, M.

Abstract

The RNA-binding protein Roquin is required to prevent autoimmunity. Roquin controls T-helper cell activation and differentiation by limiting the induced expression of costimulatory receptors such as tumor necrosis factor receptor superfamily 4 (Tnfrs4 or Ox40). A constitutive decay element (CDE) with a characteristic triloop hairpin was previously shown to be recognized by Roquin. Here we use SELEX assays to identify a novel U-rich hexaloop motif, representing an alternative decay element (ADE). Crystal structures and NMR data show that the Roquin-1 ROQ domain recognizes hexaloops in the SELEX-derived ADE and in an ADE-like variant present in the Ox40 3'-UTR with identical binding modes. In cells, ADE-like and CDE-like motifs cooperate in the repression of Ox40 by Roquin. Our data reveal an unexpected recognition of hexaloop cis elements for the posttranscriptional regulation of target messenger RNAs by Roquin.

Published
2016

15. Aberrant splicing of the tumor suppressor CYLD promotes the development of chronic lymphocytic leukemia via sustained NF-κB signaling

Author

Hahn, M, primary, Bürckert, J-P, additional, Luttenberger, C A, additional, Klebow, S, additional, Hess, M, additional, Al-Maarri, M, additional, Vogt, M, additional, Reißig, S, additional, Hallek, M, additional, Wienecke-Baldacchino, A, additional, Buch, T, additional, Muller, C P, additional, Pallasch, C P, additional, Wunderlich, F T, additional, Waisman, A, additional, and Hövelmeyer, N, additional

Published
2017
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18. Selection of higher order regression models in the analysis of multi-factorial transcription data

Author

Prazeres da Costa, O., Hoffman, A., Rey, J., Mansmann, U., Buch, T., and Tresch, A.

Subjects
Yersinia Infections, Science, Immunology, Gene Expression, Mouse Models, Biostatistics, Research and Analysis Methods, Molecular Genetics, Mice, Model Organisms, Genetics, Animals, Gene Regulation, ddc:610, Statistical Methods, Immunity to Infections, Oligonucleotide Array Sequence Analysis, Binding Sites, Gene Expression Profiling, Macrophages, Immunity, Biology and Life Sciences, Computational Biology, Genomics, Animal Models, Genome Analysis, Mice, Inbred C57BL, Genetics of Disease, Physical Sciences, Linear Models, Medicine, Regression Analysis, Genome Expression Analysis, Transcriptome Analysis, Mathematics, Statistics (Mathematics), Transcription Factors, Research Article
Abstract

IntroductionMany studies examine gene expression data that has been obtained under the influence of multiple factors, such as genetic background, environmental conditions, or exposure to diseases. The interplay of multiple factors may lead to effect modification and confounding. Higher order linear regression models can account for these effects. We present a new methodology for linear model selection and apply it to microarray data of bone marrow-derived macrophages. This experiment investigates the influence of three variable factors: the genetic background of the mice from which the macrophages were obtained, Yersinia enterocolitica infection (two strains, and a mock control), and treatment/non-treatment with interferon-γ.ResultsWe set up four different linear regression models in a hierarchical order. We introduce the eruption plot as a new practical tool for model selection complementary to global testing. It visually compares the size and significance of effect estimates between two nested models. Using this methodology we were able to select the most appropriate model by keeping only relevant factors showing additional explanatory power. Application to experimental data allowed us to qualify the interaction of factors as either neutral (no interaction), alleviating (co-occurring effects are weaker than expected from the single effects), or aggravating (stronger than expected). We find a biologically meaningful gene cluster of putative C2TA target genes that appear to be co-regulated with MHC class II genes.ConclusionsWe introduced the eruption plot as a tool for visual model comparison to identify relevant higher order interactions in the analysis of expression data obtained under the influence of multiple factors. We conclude that model selection in higher order linear regression models should generally be performed for the analysis of multi-factorial microarray data.

Published
2014

19. Correspondence: SEMA4A variation and risk of colorectal cancer

Author

Kinnersley, B. (Ben), Chubb, D. (Daniel), Dobbins, S.E. (Sara E.), Frampton, M. (Matthew), Buch, T. (Thorsten), Timofeeva, M.N. (Maria N.), Castellví-Bel, S., Farrington, S.M. (Susan), Försti, A. (Asta), Hampe, J. (Jochen), Hemminki, K. (Kari), Hofstra, R.M.W. (Robert), Northwood, J.B. (John Blackman), Palles, C. (Claire), Pinheiro, M. (Manuela), Ruiz-Ponte, C. (Clara), Schafmayer, C. (Clemens), Teixeira, M.R. (Manuel R.), Westers, H. (Helga), Wezel, T. (Tom) van, Bishop, D.T. (David Timothy), Tomlinson, I. (Ian), Dunlop, M. (Malcolm), Houlston, R. (Richard), Kinnersley, B. (Ben), Chubb, D. (Daniel), Dobbins, S.E. (Sara E.), Frampton, M. (Matthew), Buch, T. (Thorsten), Timofeeva, M.N. (Maria N.), Castellví-Bel, S., Farrington, S.M. (Susan), Försti, A. (Asta), Hampe, J. (Jochen), Hemminki, K. (Kari), Hofstra, R.M.W. (Robert), Northwood, J.B. (John Blackman), Palles, C. (Claire), Pinheiro, M. (Manuela), Ruiz-Ponte, C. (Clara), Schafmayer, C. (Clemens), Teixeira, M.R. (Manuel R.), Westers, H. (Helga), Wezel, T. (Tom) van, Bishop, D.T. (David Timothy), Tomlinson, I. (Ian), Dunlop, M. (Malcolm), and Houlston, R. (Richard)

Published
2016
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20. The IFN-gamma-Inducible GTPase, Irga6, Protects Mice against Toxoplasma gondii but Not against Plasmodium berghei and Some Other Intracellular Pathogens

Author

Liesenfeld, O., Parvanova, I., Zerrahn, J., Han, S., Heinrich, F., Munoz, M., Kaiser, F., Aebischer, T., Buch, T., Waisman, A., Reichmann, G., Utermöhlen, O., von Stebut, E., von Loewenich, F., Bogdan, C., Specht, S., Saeftel, M., Hoerauf, A., Mota, M., Könen-Waisman, S., Kaufmann, S., and Howard, J.

Subjects
parasitic diseases
Abstract

Clearance of infection with intracellular pathogens in mice involves interferon-regulated GTPases of the IRG protein family. Experiments with mice genetically deficient in members of this family such as Irgm1(LRG-47), Irgm3(IGTP), and Irgd(IRG-47) has revealed a critical role in microbial clearance, especially for Toxoplasma gondii. The in vivo role of another member of this family, Irga6 (IIGP, IIGP1) has been studied in less detail. We investigated the susceptibility of two independently generated mouse strains deficient in Irga6 to in vivo infection with T. gondii, Mycobacterium tuberculosis, Leishmania mexicana, L. major, Listeria monocytogenes, Anaplasma phagocytophilum and Plasmodium berghei. Compared with wild-type mice, mice deficient in Irga6 showed increased susceptibility to oral and intraperitoneal infection with T. gondii but not to infection with the other organisms. Surprisingly, infection of Irga6-deficient mice with the related apicomplexan parasite, P. berghei, did not result in increased replication in the liver stage and no Irga6 (or any other IRG protein) was detected at the parasitophorous vacuole membrane in IFN-gamma-induced wild-type cells infected with P. berghei in vitro. Susceptibility to infection with T. gondii was associated with increased mortality and reduced time to death, increased numbers of inflammatory foci in the brains and elevated parasite loads in brains of infected Irga6-deficient mice. In vitro, Irga6-deficient macrophages and fibroblasts stimulated with IFN-gamma were defective in controlling parasite replication. Taken together, our results implicate Irga6 in the control of infection with T. gondii and further highlight the importance of the IRG system for resistance to this pathogen.

Published
2011

21. Recurrent Coding Sequence Variation Explains only A Small Fraction of the Genetic Architecture of Colorectal Cancer

Author

Timofeeva, M.N. (Maria N.), Kinnersley, B. (Ben), Farrington, S.M. (Susan M.), Whiffin, N. (Nicola), Palles, C. (Claire), Svinti, V. (Victoria), Lloyd, A. (Amy), Gorman, M. (Maggie), Ooi, L.-Y. (Li-Yin), Hosking, F. (Fay), Barclay, E. (Ella), Zgaga, L. (Lina), Dobbins, S.E. (Sara E.), Martin, L. (Lynn), Theodoratou, E. (Evropi), Broderick, P. (Peter), Tenesa, A. (Albert), Smillie, C. (Claire), Grimes, G. (Graeme), Hayward, C. (Caroline), Campbell, A. (Archie), Porteous, D. (David), Deary, I.J. (Ian), Harris, S.E. (Sarah), Northwood, J.B. (John Blackman), Barrett, J.H. (Jennifer H.), Smith, G. (Gillian), Wolf, R. (Roland), Forman, D. (David), Morreau, H. (Hans), Ruano, D. (Dina), Tops, C. (Carli), Wijnen, J.T. (Juul), Schrumpf, M. (Melanie), Boot, A. (Arnoud), Vasen, H. (Hans), Hes, F.J. (Frederik), Wezel, T. (Tom) van, Franke, A. (Andre), Lieb, W. (Wolgang), Schafmayer, C. (Clemens), Hampe, J. (Jochen), Buch, T. (Thorsten), Propping, P. (Peter), Hemminki, K. (Kari), Försti, A. (Asta), Westers, H. (Helga), Hofstra, R.M.W. (Robert), Pinheiro, M. (Manuela), Pinto, C. (Carla), Teixeira, P.J., Ruiz-Ponte, C. (Clara), Fernández-Rozadilla, C. (Ceres), Carracedo, A. (Angel), Castells, A., Castellví-Bel, S., Campbell, H. (Harry), Bishop, D.T. (David Timothy), Tomlinson, I. (Ian), Dunlop, M.G. (Malcolm), Houlston, R. (Richard), Timofeeva, M.N. (Maria N.), Kinnersley, B. (Ben), Farrington, S.M. (Susan M.), Whiffin, N. (Nicola), Palles, C. (Claire), Svinti, V. (Victoria), Lloyd, A. (Amy), Gorman, M. (Maggie), Ooi, L.-Y. (Li-Yin), Hosking, F. (Fay), Barclay, E. (Ella), Zgaga, L. (Lina), Dobbins, S.E. (Sara E.), Martin, L. (Lynn), Theodoratou, E. (Evropi), Broderick, P. (Peter), Tenesa, A. (Albert), Smillie, C. (Claire), Grimes, G. (Graeme), Hayward, C. (Caroline), Campbell, A. (Archie), Porteous, D. (David), Deary, I.J. (Ian), Harris, S.E. (Sarah), Northwood, J.B. (John Blackman), Barrett, J.H. (Jennifer H.), Smith, G. (Gillian), Wolf, R. (Roland), Forman, D. (David), Morreau, H. (Hans), Ruano, D. (Dina), Tops, C. (Carli), Wijnen, J.T. (Juul), Schrumpf, M. (Melanie), Boot, A. (Arnoud), Vasen, H. (Hans), Hes, F.J. (Frederik), Wezel, T. (Tom) van, Franke, A. (Andre), Lieb, W. (Wolgang), Schafmayer, C. (Clemens), Hampe, J. (Jochen), Buch, T. (Thorsten), Propping, P. (Peter), Hemminki, K. (Kari), Försti, A. (Asta), Westers, H. (Helga), Hofstra, R.M.W. (Robert), Pinheiro, M. (Manuela), Pinto, C. (Carla), Teixeira, P.J., Ruiz-Ponte, C. (Clara), Fernández-Rozadilla, C. (Ceres), Carracedo, A. (Angel), Castells, A., Castellví-Bel, S., Campbell, H. (Harry), Bishop, D.T. (David Timothy), Tomlinson, I. (Ian), Dunlop, M.G. (Malcolm), and Houlston, R. (Richard)

Abstract

Whilst common genetic variation in many non-coding genomic regulatory regions are known to impart risk of colorectal cancer (CRC), much of the heritability of CRC remains unexplained. To examine the role of recurrent coding sequence variation in CRC aetiology, we genotyped 12,638 CRCs cases and 29,045 controls from six European populations. Single-variant analysis identified a coding variant (rs3184504) in SH2B3 (12q24) associated with CRC risk (OR = 1.08, P = 3.9 × 10-7), and novel damaging coding variants in 3 genes previously tagged by GWAS efforts; rs16888728 (8q24) in UTP23 (OR = 1.15, P = 1.4 × 10-7); rs6580742 and rs12303082 (12q13) in FAM186A (OR = 1.11, P = 1.2 × 10-7

Published
2015
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22. IGF1R signaling in oligodendrocytes regulates neuroinflammation without affecting cell survival

Author

Locatelli, G., Krueger, M., Ingold-Heppner, B., da Costa, O. Prazeres, Koch, L., Dolga, A., Huber, M., Gold, M., Bruening, J., Culmsee, C., Waisman, A., Bechmann, I., Becher, B., Buch, T., Locatelli, G., Krueger, M., Ingold-Heppner, B., da Costa, O. Prazeres, Koch, L., Dolga, A., Huber, M., Gold, M., Bruening, J., Culmsee, C., Waisman, A., Bechmann, I., Becher, B., and Buch, T.

Published
2015

24. A 'SWITCH-ON' T CELL RECEPTOR FOR THE INVESTIGATION OF THYMIC DEVELOPMENT

Author

Hemmer, S, Polić, B, Wunderlich, FT, Rajewsky, K, Waisman, A, Buch, T, Bernard, Alain, and Kaufmann, Stefan H.E.

Subjects
chemical and pharmacologic phenomena, T cell receptor, thymic development, positive and negative selection of T cell precursors
Abstract

Positive and negative selection of T cell precursor expressing a T cell receptor (TCR) of unknown specificity ensures that only such cells are released to the periphery that expresses a selfrestricted TCR without autoreactive specificity. Although it is of fundamental importance for the understanding of T cell differentiation and tolerance induction, only little is known about the process which allows T cell precursors to distinguish between autoreactive specificities (high avidity to self_MHC/peptide) and self-restricted specificities (intermediate avidity). To investigate this process we developed a novel mouse model that allows us to induce the expression of a defined TCR in thymocytes. The wave of cells caring the same specificity is either positively or negatively selected, dependent on the respective thymic environment. We want to use this wave to investigate in more detail the signal transduction and gene activation pathways that are involved in the thymic selection processes. To this end we have generated by gene targeting an allele of the TCR locus which carries the V J exon of the HY-TCR opposite to the transcriptional direction. By use of two antidromic loxP sites this exon can be inverted and thus expression of the HY-TCR (in conjunction with the conventional transgene for the HY chain) is made possible. To exclude the generation of other TCR a large Cre-mediated recombination event removed the TCR locus as well as all J elements. Expression of the HY-TCR chain from this modified TCR allele was confirmed by flow cytometry. To restrict Cre-mediated inversion of the ‘ HY -switch-on’ allele to the CD4CD8 positive compartment of T cell development we also generated an allele of the CD4 locus which expresses an estrogen receptor Cre fusion protein (CreERT2) that allows induction of Cre activity by injection of tamoxifen.

Published
2006

27. Re: Role of the oxidative DNA damage repair gene OGG1 in colorectal tumorigenesis

Author

Kinnersley, B. (Ben), Buch, T. (Thorsten), Castellví-Bel, S., Farrington, S.M. (Susan), Försti, A. (Asta), Hampe, J. (Jochen), Hemminki, K. (Kari), Hofstra, R.M.W. (Robert), Northwood, J.B. (John Blackman), Palles, C. (Claire), Pinheiro, M.A. (Magda Avelar), Ruiz-Ponte, C. (Clara), Schafmayer, C. (Clemens), Teixeira, P.J., Westers, H. (Helga), Wezel, T. (Tom) van, Bishop, D.T. (David Timothy), Tomlinson, I.P. (Ian), Dunlop, M.G. (Malcolm), Houlston, R. (Richard), Kinnersley, B. (Ben), Buch, T. (Thorsten), Castellví-Bel, S., Farrington, S.M. (Susan), Försti, A. (Asta), Hampe, J. (Jochen), Hemminki, K. (Kari), Hofstra, R.M.W. (Robert), Northwood, J.B. (John Blackman), Palles, C. (Claire), Pinheiro, M.A. (Magda Avelar), Ruiz-Ponte, C. (Clara), Schafmayer, C. (Clemens), Teixeira, P.J., Westers, H. (Helga), Wezel, T. (Tom) van, Bishop, D.T. (David Timothy), Tomlinson, I.P. (Ian), Dunlop, M.G. (Malcolm), and Houlston, R. (Richard)

Published
2014
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28. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2013 update

Author

Smolen, J.S. (Josef), Landewé, R.B.M. (Robert), Breedveld, F.C. (Ferdinand), Buch, T. (Thorsten), Burmester, G.R. (Gerd), Dougados, M. (Maxime), Emery, P. (Paul), Gaujoux-Viala, C. (Cécile), Gossec, L. (Laure), Nam, N. (Nguyen) van, Ramiro, S. (Sofia), Winthrop, K. (Kevin), M. de Wit (Maarten), Aletaha, D. (Daniel), Betteridge, N. (Neil), Bijlsma, J.W.J. (Hans), Boers, M. (Maarten), Buttgereit, F. (Frank), Combe, B. (Bernard), Cutolo, M. (Maurizio), Damjanov, N. (Nemanja), Hazes, J.M.W. (Mieke), Kouloumas, M. (Marios), Kvien, T.K. (Tore), Mariette, X. (Xavier), Pavelka, K. (Karel), Riel, P.L.C.M. (Piet) van, Rubbert-Roth, A. (Andrea), Scholte-Voshaar, M. (Marieke), Scott, D.L. (David), Sokka-Isler, T. (Tuulikki), Wong, J.B. (John), Heijde, D. (Desiree) van der, Smolen, J.S. (Josef), Landewé, R.B.M. (Robert), Breedveld, F.C. (Ferdinand), Buch, T. (Thorsten), Burmester, G.R. (Gerd), Dougados, M. (Maxime), Emery, P. (Paul), Gaujoux-Viala, C. (Cécile), Gossec, L. (Laure), Nam, N. (Nguyen) van, Ramiro, S. (Sofia), Winthrop, K. (Kevin), M. de Wit (Maarten), Aletaha, D. (Daniel), Betteridge, N. (Neil), Bijlsma, J.W.J. (Hans), Boers, M. (Maarten), Buttgereit, F. (Frank), Combe, B. (Bernard), Cutolo, M. (Maurizio), Damjanov, N. (Nemanja), Hazes, J.M.W. (Mieke), Kouloumas, M. (Marios), Kvien, T.K. (Tore), Mariette, X. (Xavier), Pavelka, K. (Karel), Riel, P.L.C.M. (Piet) van, Rubbert-Roth, A. (Andrea), Scholte-Voshaar, M. (Marieke), Scott, D.L. (David), Sokka-Isler, T. (Tuulikki), Wong, J.B. (John), and Heijde, D. (Desiree) van der

Published
2014
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30. 420 Analysis of genomic alterations in Ewing sarcoma (German cohort) reveals cooperating mutations and novel therapy targets

Author

Richter, G.H.S., primary, Agelopoulos, K., additional, Schmidt, E., additional, von Heyking, K., additional, Moser, B., additional, Klein, H.U., additional, Kontny, U., additional, Dugas, M., additional, Poos, K., additional, Korsching, E., additional, Buch, T., additional, Köhler, G., additional, Rössig, C., additional, Baumhoer, D., additional, Jürgens, H., additional, Burdach, S., additional, Berdel, W.E., additional, Müller-Tidow, C., additional, and Dirksen, U., additional

Published
2014
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32. Is BAC transgenesis obsolete? State of the art in the era of designer nucleases

Author

Beil, J, Fairbairn, L, Pelczar, P, Buch, T, Beil, J, Fairbairn, L, Pelczar, P, and Buch, T

Abstract

DNA constructs based on bacterial artificial chromosomes (BACs) are frequently used to generate transgenic animals as they reduce the influence of position effects and allow predictable expression patterns for genes whose regulatory sequences are not fully identified. Despite these advantages BAC transgenics suffer from drawbacks such as complicated vector construction, low efficiency of transgenesis, and some remaining expression variegation. The recent development of transcription activator-like effector nucleases (TALENs) and zinc finger nucleases (ZFNs) has resulted in new transgenic techniques which do not have the drawbacks associated with BAC transgenesis. Initial reports indicate that such designer nucleases (DNs) allow the targeted insertion of transgenes into endogenous loci by direct injection of the targeting vector and mRNA/DNA encoding the predesigned nucleases into oocytes. This results in the transgene being inserted at a specific locus in the mouse genome, thus circumventing the drawbacks associated with BAC transgenesis.

Published
2012

33. Ectopic expression of neural autoantigen in mouse liver suppresses experimental autoimmune neuroinflammation by inducing antigen-specific Tregs

Author

Lüth, S, Huber, S, Schramm, C, Buch, T, Zander, S, Stadelmann, C, Brück, W, Wraith, D C, Herkel, J, Lohse, A W, Lüth, S, Huber, S, Schramm, C, Buch, T, Zander, S, Stadelmann, C, Brück, W, Wraith, D C, Herkel, J, and Lohse, A W

Abstract

Tregs are important mediators of immune tolerance to self antigens, and it has been suggested that Treg inactivation may cause autoimmune disease. Therefore, immunotherapy approaches that aim to restore or expand autoantigen-specific Treg activity might be beneficial for the treatment of autoimmune disease. Here we report that Treg-mediated suppression of autoimmune disease can be achieved in vivo by taking advantage of the ability of the liver to promote immune tolerance. Expression of the neural autoantigen myelin basic protein (MBP) in the liver was accomplished stably in liver-specific MBP transgenic mice and transiently using gene transfer to liver cells in vivo. Such ectopic MBP expression induced protection from autoimmune neuroinflammation in a mouse model of multiple sclerosis. Protection from autoimmunity was mediated by MBP-specific CD4+CD25+Foxp3+ Tregs, as demonstrated by the ability of these cells to prevent disease when adoptively transferred into nontransgenic mice and to suppress conventional CD4+CD25- T cell proliferation after antigen-specific stimulation with MBP in vitro. The generation of MBP-specific CD4+CD25+Foxp3+ Tregs in vivo depended on expression of MBP in the liver, but not in skin, and occurred by TGF-beta-dependent peripheral conversion from conventional non-Tregs. Our findings indicate that autoantigen expression in the liver may generate autoantigen-specific Tregs. Thus, targeting of autoantigens to hepatocytes may be a novel approach to prevention or treatment of autoimmune diseases.

Published
2008

34. Gamma interferon blocks gammaherpesvirus reactivation from latency in a cell type-specific manner

Author

Steed, A, Buch, T, Waisman, A, Virgin, H W, Steed, A, Buch, T, Waisman, A, and Virgin, H W

Abstract

Gammaherpesviruses are important pathogens whose lifelong survival in the host depends critically on their capacity to establish and reactivate from latency, processes regulated by both viral genes and the host immune response. Previous work has demonstrated that gamma interferon (IFN-gamma) is a key regulator of chronic infection with murine gammaherpesvirus 68 (gammaHV68), a virus that establishes latent infection in B lymphocytes, macrophages, and dendritic cells. In mice deficient in IFN-gamma or the IFN-gamma receptor, gammaHV68 gene expression is altered during chronic infection, and peritoneal cells explanted from these mice reactivate more efficiently ex vivo than cells derived from wild-type mice. Furthermore, treatment with IFN-gamma inhibits reactivation of gammaHV68 from latently infected wild-type peritoneal cells, and depletion of IFN-gamma from wild-type mice increases the efficiency of reactivation of explanted peritoneal cells. These profound effects of IFN-gamma on chronic gammaHV68 latency and reactivation raise the question of which cells respond to IFN-gamma to control chronic gammaHV68 infection. Here, we show that IFN-gamma inhibited reactivation of peritoneal cells and spleen cells harvested from mice lacking B lymphocytes, but not wild-type spleen cells, suggesting that IFN-gamma may inhibit reactivation in a cell type-specific manner. To directly test this hypothesis, we expressed the diphtheria toxin receptor specifically on either B lymphocytes or macrophages and used diphtheria toxin treatment to deplete these specific cells in vivo and in vitro after establishing latency. We demonstrate that macrophages, but not B cells, are responsive to IFN-gamma-mediated suppression of gammaHV68 reactivation. These data indicate that the regulation of gammaherpesvirus latency by IFN-gamma is cell type specific and raise the possibility that cell type-specific immune deficiency may alter latency in distinct and important ways.

Published
2007

42. Epitope mapping and reactivity of autoantibodies to the E2 component of 2-oxoglutarate dehydrogenase complex in primary biliary cirrhosis using recombinant 2-oxoglutarate dehydrogenase complex

Author

Moteki, S, primary, Leung, P S, additional, Dickson, E R, additional, Van Thiel, D H, additional, Galperin, C, additional, Buch, T, additional, Alarcon-Segovia, D, additional, Kershenobich, D, additional, Kawano, K, additional, Coppel, R L, additional, Matuda, S, additional, and Gershwin, M E, additional

Published
1996
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