@article{ChopraBiehlSteinfattetal.2016,
  author    = {Chopra, Martin and Biehl, Marlene and Steinfatt, Tim and Brandl, Andreas and Kums, Juliane and Amich, Jorge and Vaeth, Martin and Kuen, Janina and Holtappels, Rafaela and Podlech, J{\"u}rgen and Mottok, Anja and Kraus, Sabrina and Jord{\´a}n-Garotte, Ana-Laura and B{\"a}uerlein, Carina A. and Brede, Christian and Ribechini, Eliana and Fick, Andrea and Seher, Axel and Polz, Johannes and Ottmueller, Katja J. and Baker, Jeannette and Nishikii, Hidekazu and Ritz, Miriam and Mattenheimer, Katharina and Schwinn, Stefanie and Winter, Thorsten and Sch{\"a}fer, Viktoria and Krappmann, Sven and Einsele, Hermann and M{\"u}ller, Thomas D. and Reddehase, Matthias J. and Lutz, Manfred B. and M{\"a}nnel, Daniela N. and Berberich-Siebelt, Friederike and Wajant, Harald and Beilhack, Andreas},
  title     = {Exogenous TNFR2 activation protects from acute GvHD via host T reg cell expansion},
  series = {Journal of Experimental Medicine},
  volume    = {213},
  journal   = {Journal of Experimental Medicine},
  number    = {9},
  doi       = {10.1084/jem.20151563},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-187640},
  pages     = {1881-1900},
  year      = {2016},
  abstract  = {Donor CD4\(^+\)Foxp3\(^+\) regulatory T cells (T reg cells) suppress graft-versus-host disease (GvHD) after allogeneic hematopoietic stem cell transplantation (HCT allo-HCT]). Current clinical study protocols rely on the ex vivo expansion of donor T reg cells and their infusion in high numbers. In this study, we present a novel strategy for inhibiting GvHD that is based on the in vivo expansion of recipient T reg cells before allo-HCT, exploiting the crucial role of tumor necrosis factor receptor 2 (TNFR2) in T reg cell biology. Expanding radiation-resistant host T reg cells in recipient mice using a mouse TNFR2-selective agonist before allo-HCT significantly prolonged survival and reduced GvHD severity in a TNFR2-and T reg cell-dependent manner. The beneficial effects of transplanted T cells against leukemia cells and infectious pathogens remained unaffected. A corresponding human TNFR2-specific agonist expanded human T reg cells in vitro. These observations indicate the potential of our strategy to protect allo-HCT patients from acute GvHD by expanding T reg cells via selective TNFR2 activation in vivo.},
  language  = {en}
}
@phdthesis{Berberich2012,
  author    = {Berberich, Martin},
  title     = {Rylene Bisimide-Diarylethene Photochromic Systems for Non-Destructive Memory Read-out},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-73517},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2012},
  abstract  = {Diese Doktorarbeit zeigt deutlich verbesserte aus Rylenbisimiden und Diarylethenen aufgebaute, photochrome Systeme f{\"u}r das nicht-destruktive Auslesen von Fluoreszenz. Dabei wird die Fluoreszenz der Emittereinheit durch photoinduzierten Elektronentransfer nur zu einer isomeren Form des Photochromes gel{\"o}scht. Die Triebkraft f{\"u}r den Fluoreszenz-l{\"o}schenden Elektronentransfer wurde mittels Rehm-Weller-Gleichung berechnet. Die erhaltenen Systeme erf{\"u}llen die notwendigen Anforderungen f{\"u}r ein nicht-destruktives Auslesen in einem auf Schreiben, Auslesen und L{\"o}schen basierenden fluoreszierenden Datenspeicher.},
  subject      = {Photochromie},
  language  = {en}
}
@article{MuellerQuandtMarienfeldetal.2013,
  author    = {Mueller, Kerstin and Quandt, Jasmin and Marienfeld, Ralf B. and Weihrich, Petra and Fiedler, Katja and Claussnitzer, Melina and Laumen, Helmut and Vaeth, Martin and Berberich-Siebelt, Frederike and Serfling, Edgar and Wirth, Thomas and Brunner, Cornelia},
  title     = {Octamer-dependent transcription in T cells is mediated by NFAT and \(NF-\kappa B\)},
  series = {Nucleic Acids Research},
  volume    = {41},
  journal   = {Nucleic Acids Research},
  number    = {4},
  issn      = {1362-4962},
  doi       = {10.1093/nar/gks1349},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-123280},
  pages     = {2138-2154},
  year      = {2013},
  abstract  = {The transcriptional co-activator BOB.1/OBF.1 was originally identified in B cells and is constitutively expressed throughout B cell development. BOB.1/OBF.1 associates with the transcription factors Oct1 and Oct2, thereby enhancing octamer-dependent transcription. In contrast, in T cells, BOB.1/OBF.1 expression is inducible by treatment of cells with PMA/Ionomycin or by antigen receptor engagement, indicating a marked difference in the regulation of BOB.1/OBF.1 expression in B versus T cells. The molecular mechanisms underlying the differential expression of BOB.1/OBF.1 in T and B cells remain largely unknown. Therefore, the present study focuses on mechanisms controlling the transcriptional regulation of BOB.1/OBF.1 and Oct2 in T cells. We show that both calcineurin- and \(NF-\kappa B\)-inhibitors efficiently attenuate the expression of BOB.1/OBF.1 and Oct2 in T cells. In silico analyses of the BOB.1/OBF.1 promoter revealed the presence of previously unappreciated combined NFAT/\(NF-\kappa B\) sites. An array of genetic and biochemical analyses illustrates the involvement of the \(Ca^{2+}\)/calmodulin-dependent phosphatase calcineurin as well as NFAT and \(NF-\kappa B\) transcription factors in the transcriptional regulation of octamer-dependent transcription in T cells. Conclusively, impaired expression of BOB.1/OBF.1 and Oct2 and therefore a hampered octamer-dependent transcription may participate in T cell-mediated immunodeficiency caused by the deletion of NFAT or \(NF-\kappa B\) transcription factors.},
  language  = {en}
}
@misc{SerflingAvotsKleinHesslingetal.2012,
  author    = {Serfling, Edgar and Avots, Andris and Klein-Hessling, Stefan and Rudolf, Ronald and Vaeth, Martin and Berberich-Siebelt, Friederike},
  title     = {NFATc1/alphaA: The other Face of NFAT Factors in Lymphocytes},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-75748},
  year      = {2012},
  abstract  = {In effector T and B cells immune receptor signals induce within minutes a rise of intracellular Ca++, the activation of the phosphatase calcineurin and the translocation of NFAT transcription factors from cytosol to nucleus. In addition to this first wave of NFAT activation, in a second step the occurrence of NFATc1/αA, a short isoform of NFATc1, is strongly induced. Upon primary stimulation of lymphocytes the induction of NFATc1/αA takes place during the G1 phase of cell cycle. Due to an auto-regulatory feedback circuit high levels of NFATc1/αA are kept constant during persistent immune receptor stimulation. Contrary to NFATc2 and further NFATc proteins which dampen lymphocyte proliferation, induce anergy and enhance activation induced cell death (AICD), NFATc1/αA supports antigenmediated proliferation and protects lymphocytes against rapid AICD. Whereas high concentrations of NFATc1/αA can also lead to apoptosis, in collaboration with NF-κB-inducing co-stimulatory signals they support the survival of mature lymphocytes in late phases after their activation. However, if dysregulated, NFATc1/αA appears to contribute to lymphoma genesis and - as we assume - to further disorders of the lymphoid system. While the molecular details of NFATc1/αA action and its contribution to lymphoid disorders have to be investigated, NFATc1/αA differs in its generation and function markedly from all the other NFAT proteins which are expressed in lymphoid cells. Therefore, it represents a prime target for causal therapies of immune disorders in future.},
  subject      = {Medizin},
  language  = {en}
}
@article{KleinHesslingMuhammadKleinetal.2017,
  author    = {Klein-Hessling, Stefan and Muhammad, Khalid and Klein, Matthias and Pusch, Tobias and Rudolf, Ronald and Fl{\"o}ter, Jessica and Qureischi, Musga and Beilhack, Andreas and Vaeth, Martin and Kummerow, Carsten and Backes, Christian and Schoppmeyer, Rouven and Hahn, Ulrike and Hoth, Markus and Bopp, Tobias and Berberich-Siebelt, Friederike and Patra, Amiya and Avots, Andris and M{\"u}ller, Nora and Schulze, Almut and Serfling, Edgar},
  title     = {NFATc1 controls the cytotoxicity of CD8\(^{+}\) T cells},
  series = {Nature Communications},
  volume    = {8},
  journal   = {Nature Communications},
  number    = {511},
  doi       = {10.1038/s41467-017-00612-6},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-170353},
  year      = {2017},
  abstract  = {Cytotoxic T lymphocytes are effector CD8\(^{+}\) T cells that eradicate infected and malignant cells. Here we show that the transcription factor NFATc1 controls the cytotoxicity of mouse cytotoxic T lymphocytes. Activation of Nfatc1\(^{-/-}\) cytotoxic T lymphocytes showed a defective cytoskeleton organization and recruitment of cytosolic organelles to immunological synapses. These cells have reduced cytotoxicity against tumor cells, and mice with NFATc1-deficient T cells are defective in controlling Listeria infection. Transcriptome analysis shows diminished RNA levels of numerous genes in Nfatc1\(^{-/-}\) CD8\(^{+}\) T cells, including Tbx21, Gzmb and genes encoding cytokines and chemokines, and genes controlling glycolysis. Nfatc1\(^{-/-}\), but not Nfatc2\(^{-/-}\) CD8\(^{+}\) T cells have an impaired metabolic switch to glycolysis, which can be restored by IL-2. Genome-wide ChIP-seq shows that NFATc1 binds many genes that control cytotoxic T lymphocyte activity. Together these data indicate that NFATc1 is an important regulator of cytotoxic T lymphocyte effector functions.},
  language  = {en}
}
@article{StaussBrunnerBerberichSiebeltetal.2016,
  author    = {Stauss, Dennis and Brunner, Cornelia and Berberich-Siebelt, Friederike and H{\"o}pken, Uta E. and Lipp, Martin and M{\"u}ller, Gerd},
  title     = {The transcriptional coactivator Bob1 promotes the development of follicular T helper cells via Bcl6},
  series = {Embo Journal},
  volume    = {35},
  journal   = {Embo Journal},
  number    = {8},
  doi       = {10.15252/embj.201591459},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-189506},
  pages     = {881-898},
  year      = {2016},
  abstract  = {Follicular T helper (Tfh) cells are key regulators of the germinal center reaction and long-term humoral immunity. Tfh cell differentiation requires the sustained expression of the transcriptional repressor Bcl6; however, its regulation in CD4\(^+\) T cells is incompletely understood. Here, we report that the transcriptional coactivator Bob1, encoded by the Pou2af1 gene, promotes Bcl6 expression and Tfh cell development. We found that Bob1 together with the octamer transcription factors Oct1/Oct2 can directly bind to and transactivate the Bcl6 and Btla promoters. Mixed bone marrow chimeras revealed that Bob1 is required for the expression of normal levels of Bcl6 and BTLA, thereby controlling the pool size and composition of the Tfh compartment in a T cell-intrinsic manner. Our data indicate that T cell-expressed Bob1 is directly involved in Tfh cell differentiation and required for mounting normal T cell-dependent B-cell responses.},
  language  = {en}
}