@article{HennigMichalskiRutkowskietal.2018,
  author    = {Hennig, Thomas and Michalski, Marco and Rutkowski, Andrzej J. and Djakovic, Lara and Whisnant, Adam W. and Friedl, Marie-Sophie and Jha, Bhaskar Anand and Baptista, Marisa A. P. and L'Hernault, Anne and Erhard, Florian and D{\"o}lken, Lars and Friedel, Caroline C.},
  title     = {HSV-1-induced disruption of transcription termination resembles a cellular stress response but selectively increases chromatin accessibility downstream of genes},
  series = {PLoS Pathogens},
  volume    = {14},
  journal   = {PLoS Pathogens},
  number    = {3},
  doi       = {10.1371/journal.ppat.1006954},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-176350},
  pages     = {e1006954},
  year      = {2018},
  abstract  = {Lytic herpes simplex virus 1 (HSV-1) infection triggers disruption of transcription termination (DoTT) of most cellular genes, resulting in extensive intergenic transcription. Similarly, cellular stress responses lead to gene-specific transcription downstream of genes (DoG). In this study, we performed a detailed comparison of DoTT/DoG transcription between HSV-1 infection, salt and heat stress in primary human fibroblasts using 4sU-seq and ATAC-seq. Although DoTT at late times of HSV-1 infection was substantially more prominent than DoG transcription in salt and heat stress, poly(A) read-through due to DoTT/DoG transcription and affected genes were significantly correlated between all three conditions, in particular at earlier times of infection. We speculate that HSV-1 either directly usurps a cellular stress response or disrupts the transcription termination machinery in other ways but with similar consequences. In contrast to previous reports, we found that inhibition of Ca\(^{2+}\) signaling by BAPTA-AM did not specifically inhibit DoG transcription but globally impaired transcription. Most importantly, HSV-1-induced DoTT, but not stress-induced DoG transcription, was accompanied by a strong increase in open chromatin downstream of the affected poly(A) sites. In its extent and kinetics, downstream open chromatin essentially matched the poly(A) read-through transcription. We show that this does not cause but rather requires DoTT as well as high levels of transcription into the genomic regions downstream of genes. This raises intriguing new questions regarding the role of histone repositioning in the wake of RNA Polymerase II passage downstream of impaired poly(A) site recognition.},
  language  = {en}
}
@article{VendelovaAshourBlanketal.2018,
  author    = {Vendelova, Emilia and Ashour, Diyaaeldin and Blank, Patrick and Erhard, Florian and Saliba, Antoine-Emmanuel and Kalinke, Ulrich and Lutz, Manfred B.},
  title     = {Tolerogenic transcriptional signatures of steady-state and pathogen-induced dendritic cells},
  series = {Frontiers in Immunology},
  volume    = {9},
  journal   = {Frontiers in Immunology},
  number    = {333},
  doi       = {10.3389/fimmu.2018.00333},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-175636},
  year      = {2018},
  abstract  = {Dendritic cells (DCs) are key directors of tolerogenic and immunogenic immune responses. During the steady state, DCs maintain T cell tolerance to self-antigens by multiple mechanisms including inducing anergy, deletion, and Treg activity. All of these mechanisms help to prevent autoimmune diseases or other hyperreactivities. Different DC subsets contribute to pathogen recognition by expression of different subsets of pattern recognition receptors, including Toll-like receptors or C-type lectins. In addition to the triggering of immune responses in infected hosts, most pathogens have evolved mechanisms for evasion of targeted responses. One such strategy is characterized by adopting the host's T cell tolerance mechanisms. Understanding these tolerogenic mechanisms is of utmost importance for therapeutic approaches to treat immune pathologies, tumors and infections. Transcriptional profiling has developed into a potent tool for DC subset identification. Here, we review and compile pathogen-induced tolerogenic transcriptional signatures from mRNA profiling data of currently available bacterial- or helminth-induced transcriptional signatures. We compare them with signatures of tolerogenic steady-state DC subtypes to identify common and divergent strategies of pathogen induced immune evasion. Candidate molecules are discussed in detail. Our analysis provides further insights into tolerogenic DC signatures and their exploitation by different pathogens.},
  language  = {en}
}