@article{WarnckeVogtUlrichetal.2004, author = {Warncke, Max and Vogt, Birgit and Ulrich, Jacqueline and von Laer, Meike Dorothee and Beyer, Winfried and Klump, Hannes and Micheel, Burkhard and Sheriff, Ahmed}, title = {Efficient in vitro transduction of naive murine B cells with lentiviral vectors}, year = {2004}, abstract = {The aim of this study was to determine the impact of lentiviral transduction on primary murine B cells. Studying B cell activities in vivo or using them for tolerance induction requires that the cells remain unaltered in their biological behavior except for expression of the transgene. As we show here, murine B cells can efficiently be transduced by lentiviral, VSV-G-pseudotyped vectors without the necessity of prior activation. Culture with LPS gave enhanced transduction efficiencies but led to the upregulation of CD86 and proliferation of the cells. Transduction of naive B cells by lentiviral vectors was dependent on multiplicity of infection and did not lead to a concomitant activation. Furthermore, the transduced cells could be used for studies in the NOD mouse system without altering the onset of diabetes. We conclude that lentiviral gene transfer into naive B cells is a powerful tool for manipulation of B cells for therapeutic applications.}, language = {en} } @article{SchenkMatyssekMicheel2004, author = {Schenk, J{\"o}rg A. and Matyssek, Franziska and Micheel, Burkhard}, title = {Interleukin 4 increases the antibody response against Rubisco in mice}, year = {2004}, abstract = {The influence of interleukin 4 (IL-4) on antibody titer in serum and spleen culture supernatant in mice immunized with spinach (Spinacia oleracea L.) Rubisco was investigated. Therefore, we boosted one mouse additionally to the antigen with recombinant mouse IL-4. We found that the Rubisco-specific antibody titer in serum as well as in spleen cell culture supernatant was significantly enhanced in the IL-4 mouse. Most of the antibodies were of the IgG1 subclass. After hybridoma generation, Rubisco-specific antibodies were found in more than 95\% of the wells tested compared to about 12\% of the control mouse.}, language = {en} } @article{JandrigSeitzHinzmannetal.2004, author = {Jandrig, Burkhard and Seitz, Susanne and Hinzmann, Bernd and Arnold, Wolfgang and Micheel, Burkhard and Koelble, Konrad and Siebert, Reiner and Schwartz, Arnfried and Ruecker, Karin and Schlag, Peter M. and Scherneck, Siegfried and Rosenthal, Andra}, title = {ST18 is a breast cancer tumor suppressor gene at human chromosome 8q11.2}, year = {2004}, abstract = {We have identified a gene, ST18 (suppression of tumorigenicity 18, breast carcinoma, zinc-finger protein), within a frequent imbalanced region of chromosome 8q11 as a breast cancer tumor suppressor gene. The ST18 gene encodes a zinc-finger DNA-binding protein with six fingers of the C2HC type (configuration Cys-X5-Cys-X12-His-X4-Cys) and an SMC domain. ST18 has the potential to act as transcriptional regulator. ST18 is expressed in a number of normal tissues including mammary epithelial cells although the level of expression is quite low. In breast cancer cell lines and the majority of primary breast tumors, ST18 mRNA is significantly downregulated. A 160 bp region within the promoter of the ST18 gene is hypermethylated in about 80\% of the breast cancer samples and in the majority of breast cancer cell lines. The strong correlation between ST18 promoter hypermethylation and loss of ST18 expression in tumor cells suggests that this epigenetic mechanism is responsible for tumor-specific downregulation. We further show that ectopic ST18 expression in MCF-7 breast cancer cells strongly inhibits colony formation in soft agar and the formation of tumors in a xenograft mouse model}, language = {en} }