@article{RiquelmeHaarerKammleretal.2018,
  author    = {Riquelme, Paloma and Haarer, Jan and Kammler, Anja and Walter, Lisa and Tomiuk, Stefan and Ahrens, Norbert and Wege, Anja K. and Goecze, Ivan and Zecher, Daniel and Banas, Bernhard and Spang, Rainer and F{\"a}ndrich, Fred and Lutz, Manfred B. and Sawitzki, Birgit and Schlitt, Hans J. and Ochando, Jordi and Geissler, Edward K. and Hutchinson, James A.},
  title     = {TIGIT\(^+\) iTregs elicited by human regulatory macrophages control T cell immunity},
  series = {Nature Communications},
  volume    = {9},
  journal   = {Nature Communications},
  number    = {9},
  doi       = {10.1038/s41467-018-05167-8},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-226321},
  pages     = {2858, 1-18},
  year      = {2018},
  abstract  = {Human regulatory macrophages (Mreg) have shown early clinical promise as a cell-based adjunct immunosuppressive therapy in solid organ transplantation. It is hypothesised that recipient CD4(+) T cell responses are actively regulated through direct allorecognition of donor-derived Mregs. Here we show that human Mregs convert allogeneic CD4(+) T cells to IL-10-producing, TIGIT(+) FoxP3(+)-induced regulatory T cells that non-specifically suppress bystander T cells and inhibit dendritic cell maturation. Differentiation of Mreg-induced Tregs relies on multiple non-redundant mechanisms that are not exclusive to interaction of Mregs and T cells, including signals mediated by indoleamine 2,3-dioxygenase, TGF-beta, retinoic acid, Notch and progestagen-associated endometrial protein. Preoperative administration of donor-derived Mregs to living-donor kidney transplant recipients results in an acute increase in circulating TIGIT(+) Tregs. These results suggest a feed-forward mechanism by which Mreg treatment promotes allograft acceptance through rapid induction of direct-pathway Tregs.},
  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}
}
@article{SchiererOstaleckiZinseretal.2018,
  author    = {Schierer, Stefan and Ostalecki, Christian and Zinser, Elisabeth and Lamprecht, Ricarda and Plosnita, Bianca and Stich, Lena and Doerrie, Jan and Lutz, Manfred B and Schuler, Gerold and Baur, Andreas S},
  title     = {Extracellular vesicles from mature dendritic cells (DC) differentiate monocytes into immature DC},
  series = {Life Science Alliance},
  volume    = {1},
  journal   = {Life Science Alliance},
  number    = {6},
  doi       = {10.26508/lsa.201800093},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-228587},
  pages     = {e201800093, 1-17},
  year      = {2018},
  abstract  = {During inflammation, murine and human monocytes can develop into dendritic cells (DC), but this process is not entirely understood. Here, we demonstrate that extracellular vesicles (EV) secreted by mature human DC (maDC) differentiate peripheral monocytes into immature DC, expressing a unique marker pattern, including 6-sulfo LacNAc (slan), Zbtb46, CD64, and CD14. While EV from both maDC and immature DC differentiated monocytes similar to GM-CSF/IL-4 stimulation, only maDC-EV produced precursors, which upon maturation stimulus developed into T-cell-activating and IL-12p70-secreting maDC. Mechanistically, maDC-EV induced cell signaling through GM-CSF, which was abundant in EV as were IL-4 and other cytokines and chemokines. When injected into the mouse skin, murine maDC-EV attracted immune cells including monocytes that developed activation markers typical for inflammatory cells. Skin-injected EV also reached lymph nodes, causing a similar immune cell infiltration. We conclude that DC-derived EV likely serve to perpetuate an immune reaction and may contribute to chronic inflammation.},
  language  = {en}
}